Just did this workout With Kelly Anne DeCollibus. It was a fun workout (not for her!) and she looks great doing it.  She’s a real trooper in the gym and has the ‘never say die’ attitude, and I know some guys who would not survive this workout at the pace and loads used. This workout was clearly in the “no pink dumbbells zone” and women should pay close attention there. Put down the tiny dumbells, get away from the endless low intensity aerobics, and you’ll see big improvements in your body and spend less time in the gym.

I do this exact program when the mood hits, and yes, use higher loads, but it floors me every time. This gal never fails to impress me with her strength and willingness to give it her all what ever gets thrown at her, which is a quality I demand of people when I work with them.

Whole Body Conditioning/GPP Day With Kelly D! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

SO YOU’RE A MOM. Maybe you’re a new one, or one with a toddler, or one or two (or more!) children around. Your life is busy. I know, I get it.  And as a trainer, a mom, and a trainer TO moms, I’ve heard more than my fair share of excuses (some good, and some bad) of why some mommies just can’t take the time or make the effort to hit the weights, get to the gym, work out in the home, and exercise.  Here’s what I’ve heard, and here’s how to fix it.

1. I have no time. BUSTED: Set your alarm clock earlier, cut out pointless behaviors (watching TV, surfing the internet), work out when baby naps, involve baby in your daily walks, take a mommy and me stroller class (or something similar), make exercise a priority, budget your time better, leave the dishes in the sink, or hire a housekeeper to free up some time.  Seriously, if you can’t take 3 or 4 hours out of every week to dedicate to fitness and wellness, that’s saying something about how you value your own health.

2. I’m too tired. BUSTED: Take a good long look at your diet. Are you getting in proper nutrition? You could be deficient in a vitamin, not eating enough, not drinking enough water, or are simply choosing foods that make you feel sluggish.  Consider supplementing with a multivitamin, or if you handle stimulants fine, a cup of green tea or coffee.  Try a little bit of cardio early in the morning before the family wakes up; it gets the blood pumping and is an instant pick-me-up. Then take a nap while hubby watches baby.

3. I’m intimidated by getting in the weight room, I’m self conscious of my body, and I’m still in maternity clothes. BUSTED: You don’t have to go to a commercial gym.  It took you 9 months to complete your pregnancy, so the weight will take time to come off.  If you can’t make it to the gym, invest in some resistance bands and light dumbbells at home. Newbies and even those with some training under the belt (if you are coming off a pregnancy, you’re likely to be a little deconditioned) will experience some terrific gains in strength (and not mass) after an extended layoff.  Readers who have lifted and remember the beginning phase know what I’m talking about; milk the newbie period for all it’s worth. The payoff will be increased muscle tone and a stronger, firmer body.

4. I have no motivation to exercise. BUSTED: Find a training partner, enlist the help of a friend, hire a personal trainer, an online diet coach, and be accountable to SOMEONE.  Someone you pay, or someone who is waiting for you at the trail for a walk. Social networks are becoming increasingly popular, get on Facebook and announce your goals publicly (I want to lose the baby weight, help me stay on track!) and see how many friends can help you stick to it.

5. I’m a mom and therefore I must put my family first; I feel guilty about taking the time to exercise. BUSTED: Just ask your husband/boyfriend/partner if he feels guilty about spending Sunday afternoon on the couch watching football while you entertain and distract Junior for a few hours. Yes, your children, family, and husband need to know you will be there for them.  You’re a parent and you always will be.  Life will be hectic from now on. But exercise, be it a 20-minute walk, or 30 minutes of strength training, a workout DVD at home, are great stress relievers. So take time to destress with physical activity. You’ll be doing everyone a favor, because raising a family, working a job, being a wife, and a mom is plenty stressful.

-Sumi Singh is a Personal Trainer in Austin, TX and an online diet coach. Her website is www.shailafitness.com

Top 5 Excuses Moms Give to Avoid Exercise, and How To Fix It is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Training after 40 and beyond! I get asked all the time about training after 40;  asked if I would do a vid or write an article on what, if any, differences people over 40 years old should focus on regarding their training. I cover the topic below in this latest vid.

Training After 40! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

As promised, the follow-up article to personal my eating disorder story will cover the science behind anorexia nervosa and bulimia nervosa. Now, I know that getting into technical terms may seem overwhelming. Below I’ve tried to simplify this as much as possible for you, and I’ve highlighted the most important things you should know, how it affects you, and why it matters.

Before we dive in, though, a few terms….

Neurotransmitter: a chemical messenger facilitates communication between the brain and the rest of your body

Neuropeptides: small protein-esque molecules that communicate with one another via neurons

ANOREXIA NERVOSA is a mental illness characterized by distorted body image, significant reduction in food consumption, over-obsession with food and body weight, and extreme weight loss. Over 90 percent of victims are young adult females. It is believed that an individual’s social environment contributes significantly to the development of eating disorders, particularly the idea that being thin equates with beauty. An individual must be at the 85^th percentile or below the normal weight for his/her age and height, be deathly afraid of gaining weight, have distorted body image and be in denial about his/her condition, and have not have menstruated for at least three cycles to be diagnosed with this disorder.[1]

BULIMIA NERVOSA involves consuming copious amounts of food in a short period of time (binging) followed by attempts to get rid of the food somehow (purging), usually by self-induced vomiting or taking laxatives. While binging, person often feels a loss of control over the food. It is not uncommon for patients to fall within the normal weight range or even be slightly overweight. In order to be diagnosed, an individual must also been binging and purging at least twice a week for a minimum of three months.

Evidence suggests that increased serotonin activity in the brain is responsible for anorexic tendencies (ie. appetite suppression)[2]. Those with anorexia nervosa frequently exhibit certain personality traits, including perfectionism, anxiety, low self-esteem, and social isolation. It is not uncommon for those individuals to be top-level students and athletes[3].

Serotonin

Serotonin is a neurotransmitter that plays a role in a multitude of behaviors, including hunger, impulse control, aggressive behavior, depression, perception, and anxiety. High levels can contribute to a sense of constant anxiety, and severely restricting calories to the point of starvation can engender a calming response. On the other hand, low levels lends to a sense of depression, and binging can temporarily alleviate the sensation. Erratic eating behaviors (both under-eating and overeating) can lead to a disruption in serotonin levels.

A 2005 study found that altered serotonin levels continue to persist over a year after patients have recovered from anorexia nervosa[4]. For those who participated in bulimia-type anorexia, there was increased activity in a specific serotonin receptor; for those recovering from restrictive-type anorexia, receptor hyperactivity was linked to anxiety.

Why does this matter? While serotonin disruptions do have a genetic component, our behaviors can bring about this abnormality as well. Irregular levels can also be found in those with other mental disorders such as obsessive compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, and borderline personality disorder. This may explain why we tend to find individuals with eating disorders to possess obsessive, perfectionistic personality traits.

This describes how I was to a T. In the thick of my eating disorder, I would start school papers weeks before they were due, comb through every textbook multiple times to stay ahead of the readings, and snap if my day didn’t unfold exactly as planned.

Dopamine

Dopamine is another well-known neurotransmitter that I’m sure you’ve all heard of. It’s associated with novelty-seeking, motor activity, and rewards. Dopamine is released when an individual experiences something rewarding or pleasurable, such as food, sex, or drugs.

This is interesting. A brain imaging study published in 2011 in Obesity looked at the difference between obese subjects and binge eaters[5]. Binge eaters were found to have significantly increased dopamine levels in the presence of their favorite foods and a drug called methylphenidate, which blocks the reuptake of dopamine, as compared to the control group, but the same increase was not observed in other conditions (neutral stimulation with and without methylphenidate, and food stimulation without methylphenidate). This dopamine response occurred in the region of the brain called the caudate, which is associated with preparing the brain to seek the reward (in this case, food), but not necessarily process it. This might explain why binge eaters get so excited at the sight of pasta, cereal, and donuts, yet the actual experience of inhaling the food in a panicked frenzy is a blur.

Dopamine receptors, best known for their association with reinforcement and reward, are also linked to eating disorders: increased receptor binding was found in those with a history of anorexia nervosa as compared to healthy women[6]. These changes in the dopamine system may alter the perceived value of rewards, such as individuals with anorexia nervosa who are obsessed with abstaining from food.

For most people, eating is supposed to be a pleasurable experience. For those with anorexia nervosa or bulimia nervosa, however, the opposite is true: eating becomes an anxiety-filled affair, wrought with negative thoughts. A UCSD study used amphetamine, a drug that release dopamine in the brain, to investigate this phenomenon. In healthy women, amphetamine-induced dopamine release was associated with pleasure. But as predicted, amphetamine in those suffering from anorexia nervosa resulted in activation of the part of the brain that harbors worries[7]. This biological reason explains why it is so difficult for anorexic patients to consume food; they simply experience the opposite reactions to food from the rest of the population.

I know this sensation. In my dark days, whenever my stomach growled and begged for sustenance, I felt happy. There was this odd sense of empowerment that overcame me and only made me want to continue depriving myself of food. Remember that part when I talked about how I was forced to eat out with my family and how anxious that made me? Yep, dopamine played a key role right there. Once my bulimia came in full-force, the only thing that would stop me from consuming every sugary carb in sight was having other people around me. My hypersensitivity to the way others’ views me was enough to deter, or at least temporarily stall, my binge eating tendencies.

Neuropeptide Y (NPY)

Neuropeptide Y is a pancreatic peptide that increases food intake. NPY injected into the hypothalamus of rodents has led to increased appetite, and animal models of obesity have been found to have higher-than-normal levels of NPY[8]. Stressful circumstances can also elevate circulating levels, as can food deprivation[9].

Patients with anorexia nervosa have higher CSF concentrations of NPY, which may indicate a response to the chronic lack of food. Long-term recovered patients, however – such as myself – did not have NPY levels that differed from the control values[10].  This could be a reflection of at least some of the body’s signals reverting back to their normal functioning.  The same phenomenon was not observed in patients with bulimia nervosa – in fact, studies reported different results here.

SUMMING IT UP

This article is by no means a comprehensive review of the science behind eating disorders – but it’s a start. There are many, many hormones and neuropeptides that I’ve left out here for the sake of keeping things as simple as possible.

I will say one more thing, though. Never underestimate the influence of the surrounding environment. The culture in which you are raised, the expectations to which you are held, the images you are bombarded with on a daily basis… they have a way of working into your subconscious and affecting just about every decision you make. I know this. In fact, I’d venture to say that environmental factors play an even greater role in your risk of developing an eating disorder than anything else.

Unfortunately, we still don’t fully understand what exactly causes eating disorders. We know some, not all, of what goes on in our bodies – and even then, we’re not entirely sure. I’d like to better understand this issue myself. But until then, I can find comfort in the fact that I know there are scientists out there continually seeking to dig deeper and find answers. Eating disorders will likely never completely cease to exist, but as long as we keep striving to take steps forward and continue to increase awareness, I think we’ll manage alright.

[1] “Anorexia Nervosa.” U.S. National Library of Medicine. April 11 2011. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001401/

[2] Hellew, Lauren. “Biochemical Correlates of Anorexia and Bulimia.” Serendip. January 4 2008. http://serendip.brynmawr.edu/exchange/node/1727

[3] “Mental Illness: Anorexia Nervosa.” National Alliance on Mental Illness. http://www.nami.org/Template.cfm?Section=By_Illness&template=/ContentManagement/ContentDisplay.cfm&ContentID=102975

[4] Kaye WH, Bailer UF, Frank GK et al. “Brain imaging of serotonin after recovery from anorexia and bulimia nervosa.” Physiology & Behavior. September 15 2005. Volume 86, pp. 15-17.

[5] Gene-Jack Wang, Allan Geliebter, Nora D. Volkow, Frank W. Telang, Jean Logan, Millard C. Jayne, Kochavi Galanti, Peter A. Selig, Hao Han, Wei Zhu, Christopher T. Wong, Joanna S. Fowler. Enhanced Striatal Dopamine Release During Food Stimulation in Binge Eating Disorder. Obesity, 2011; DOI: 10.1038/oby.2011.27

[6] University of Pittsburgh Medical Center. “Specific Regions Of Brain Implicated In Anorexia Nervosa, Finds Univ. Of Pittsburgh Study.” ScienceDaily, 8 Jul. 2005. Web. 22 Nov. 2011.

[7] Bailer, U. F., Narendran, R., Frankle, W. G., Himes, M. L., Duvvuri, V., Mathis, C. A. and Kaye, W. H. (2011), Amphetamine induced dopamine release increases anxiety in individuals recovered from anorexia nervosa. International Journal of Eating Disorders. doi: 10.1002/eat.20937

[8] Erickson JC, Hollopeter G, Palmiter RD. Attenuation of the obesity syndrome of ob/ob mice by the loss of neuropeptide Y. Science. 1996;273:1704-1707.

[9] Kalra SP, Dube MG, Sahu A, Phelps CP, Kalra PS. Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food. Proc Natl Acad Sci USA. 1991;88:10931-10935.

[10] Baranowska B, Wolinska-Witort E, Wasilewska-Dziubinska E, Roguski K, Chmielowska M. Plama leptin, neuropeptide Y (NPY) and galanin concentrations in bulimia nervosa and in anorexia nervosa. Neuroendocrinol Lett. 2001;22:356-358.

[11] Otto B, Cuntz U, Fruehauf E, et al. Weight gain decreases elevated plasma ghrelin concentrations of patietns with anorexia nervosa. Eur J Endocrinol. 2001;145:669-673.

[12] Tollie V, Kadem M, Bluet-Pajot MT, et al. Balance in ghrelin and leptin plasma levels in anorexia nervosa patients and constitutionally thin women. J Clin Endocrinol Metab. 2003;88:109-116.

[13] Jimerson DC, Wolfe BE. Eating disorders: neurobiology and symptomatology. In: Asbury AK, McKhann GM, McDonald WI, Goadsby PJ, McArthur JC, eds. Diseases of the Nervous System: Clinical Neursocience and Therapeutic Principles. 3^rd ed. Cambridge, UK: Cambridge University Press; 2002:808-815.

The Science Behind Eating Disorders is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Latest vid from Panama: Leg day with Fitness Model Ariadna González Fontelio!

Leg Day with Fitness Model Ariadna González Fontelio! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Does Your Mind Stop You From Losing Weight?

It’s interesting to note;  the single most important factor to not just getting the weight off, but keeping it off, is between our ears. That is, how people approach the issue, psychologically speaking,  is an essential component of success. And yet, 8 zillion weight loss books and programs out there, and at best, this aspect of weight loss gets lip service only.

Many diet programs out there don’t address the psychological aspect of why people fail to be successful with long-term weight loss. However, quite a few studies exist that have looked at just that. In many respects, the psychological aspect is the most important for long-term weight loss, and probably the most underappreciated component.

Studies that compare the psychological characteristics of people who have successfully kept the weight off to people who have regained the weight, see clear differences between these two groups. For example, one study that looked at 28 obese women who had lost weight but regained the weight that they had lost, compared to 28 formerly obese women who had lost weight and maintained their weight for at least one year and 20 women with a stable weight in the healthy range, found the women who regained the weight:

• Had a tendency to evaluate self-worth in terms of weight and shape

• Had a lack of vigilance with regard to weight control

• Had a dichotomous (black-and-white) thinking style

• Had the tendency to use eating to regulate mood.

The researchers concluded:

“The results suggest that psychological factors may provide some explanation as to why many people with obesity regain weight following successful weight loss.”

This particular study was done on women, so it reflects some of the specific psychological issues women have – but make no mistake here – men also have their own psychological issues that can sabotage their long term weight loss efforts. (6)

Additional studies on men and women find psychological characteristics such as “having unrealistic weight goals, poor coping or problem-solving skills and low self-efficacy” often predict failure with long term weight loss. (7) On the other hand, psychological traits common to people who experienced successful long term weight loss include “…an internal motivation to lose weight, social support, better coping strategies and ability to handle life stress, self-efficacy, autonomy, assuming responsibility in life, and overall more psychological strength and stability.” (8)

The main point of this section is to illustrate that psychology plays a major role in determining if people are successful with long-term weight loss. If it’s not addressed as part of the overall plan, it can be the factor that makes or breaks your success. This, however, is not an area most nutrition programs can adequately tackle and should not be expected to. However, the better programs do generally attempt to help with motivation, goal setting, and support. Lack of support is one important issue I identified early, having personally trained so many people, and getting feedback from my articles, etc. That’s why my weight loss program comes with a private forum where people can get support, advice, and get answers to their questions.

If you see yourself in the above lists from the groups that failed to maintain their weight long term, then know you will need to address those issues via counseling, support groups, etc. Don’t expect any weight loss program to cover this topic adequately but do look for programs that attempt to offer support, goal setting, and resources that will keep you on track.

Note: the above is a modified section from a longer article called “The Big Picture of Permanent Weight Loss.” More info on the topic of successful long term weight loss, the citations from the studies mentioned above, etc can be found in that article if interested.

Psychology 101 of Weight Loss is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Having worked in the fitness industry for over 10 years now, what I’ve learned from watching the trends is that one particular trend or “guru” will claim that their way is the only way to get fit or achieve your fitness goals.  Even if that means you MUST supplement with some plant extract or completely eliminate grains and any thing that looks like a carb from your diet, the ONLY way to achieve fitness superstardom is by following a straight, linear path.

Not every workout requires pumped-up muscles and gut busting weights. Stick with a lifetime approach to fitness.

I love fitness, but it’s not a religion. You aren’t always going to walk the straight and narrow, and nor do you have to. It’s perfectly fine to do a mix of low intensity and high-intensity cardiovascular work, for instance. Not every single workout requires interval training, high-intensity interval training, tabatas, and the like. If your body wants to crank out some moderate steady state cardiovascular activity without dripping buckets of sweat, you’re still doing a whole lot better than if you had done absolutely nothing.

Along the same lines, not every workout in the weight room needs to translate into the requisite day-after (or two days-after) muscle soreness.  Bodybuilders popularized workout splits that might have them in the gym 6 days a week, but beginner trainees can see results with as little as 2 to 3 times per week full body workouts.

And sometimes, an “easy” workout is appropriate. Though they’re not always my favorite, every once in a while, I have one. Maybe I slept poorly because a certain toddler had a nightmare, maybe I’m stressed, or maybe I simply am getting older, but I’ve had workouts where I feel like I’ve made little progress (e.g., not progressing in terms of weight). Nevertheless, I got it my workout in, took some time for myself, and did something other than complain that I’m stressed or just don’t have the time.

Just like exercise should not equal suffering, weight loss needn’t be an exercise in total deprivation. If you’ve packed on the weight and need to lose it in an absolute hurry to fit in your bridal dress or make weight for some athletic competition, that’s one thing. Perhaps a rapid approach to fat loss or slashing carbs might be a way for you to lose weight (and water weight) in a hurry. But just because you’ve heard that diet works super-fast does not mean it’s best for you. Most of my client success stories feature people that have lost the weight (and more importantly, kept the weight off) because their overall approach was more reasonable.  How? By using baby steps, incremental changes, persistence, dedication, forming better habits, lifting weights, and adding in moderate amounts of cardiovascular activity.  Their approach was somewhere in the middle.

Here’s my point; you don’t need to kill yourself in the gym, slog through daily hour long cardio sessions, or avoid every single gram of carbohydrate to improve your strength, shed some fat, and improve your figure. The face of health and fitness is changing.  I see more and more elderly trainees, post-natal moms, first-time lifters in their 40s and above, and other beginners making serious gains and progress by keeping their approach moderate and their goals long-term.

And while your progress may not always be dramatic on the scale, your shirt soaking wet, or your muscles rippled and hard, the changes that are going on are undeniable.  The middle of the road approach might not be exciting but it’s reasonable, doable, and achievable—and might be the road for you.

-Sumi Singh is a Personal Trainer in Austin, TX and an online diet coach. Her website is www.shailafitness.com

Why A Moderate Approach Might Be Best is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

As we get older, get busy with families and work, go to one too many office parties, happy hours, and cupcake shops, we often don’t notice the slow creeping on of pounds. Or maybe we do. Or maybe you wake up one day and can’t get the jeans to fit or the shirt over your bellybutton. Short of buying an entire wardrobe, you’re faced with a dilemma.

Understandably, the last thing most of us want to do is go on a diet or reduce calories. The very thought of doing so sends some of us into a tailspin, feasting “last supper” style, or running to the donut store before we begin a weight loss diet “tomorrow.” The good news is that you can make gradual, small changes and lose weight effortlessly. The same way you allowed small changes in your diet that added the pounds on gradually (the extra wine at happy hour, the chocolate kisses at the front desk, the cupcake at the birthday party, the desert you could have split, the caramel machiatto, etc), is the same way you can effortlessly lose weight by making small changes.

Always try to sit down to enjoy your meal, rather than eating on the go.

You can start by making these changes at home, and in the kitchen. This is where a lot of mindless behaviors are created. Think about it; you get home from work, it’s been hours since you ate and you inhale a bag of chips and party nuts before you’ve even started dinner. Or you sit in front of the TV to watch the game and chug a few beers and happen to order a pizza that you’ve devoured and don’t even remember it. Or you wolf down some Girl Scout cookies you bought for (or from!) your kid, because it’s “there.”

And at the end of the day/week/year you’ve consumed a bunch more calories than you remember, and simply ate more than you thought. Mindless eating is a big problem when you’re busy and on the go all the time (most of us). So, what can we do eat mindfully, and thereby lose some weight effortlessly?

1) Make the declaration vocal: Say: “I’m not hungry but I am going to eat this anyway.” It makes you sound silly, and possibly greedy too. Honor real hunger, not a suggestion from a commercial.

2) Think 20% less “other stuff,” 20% more veggies. Take a look at your dinner plate. Could you trim off a small amount of the extra pork loin, or a portion of your pasta, and replace it with some grilled or green leafy vegetables?

3) We eat with our eyes, so visual cues for portion sizes are important to repeat. If like my dog, you’re capable of licking up entire jars of peanut butter or for eating an entire tin of nuts, perhaps it’s better you start buying the single serving peanut butter packets or those 100-calorie packages of nuts/snacks. Some people will just portion out the tin of nuts into mini ziplock baggies to cue their appetites when their eyes are done eating.

4) Volumize your food to make it look bigger. I’m not talking about taking a hair dryer to your bowl of oatmeal, BUT you could do things like lessen the amount of ground beef you consume in a burger patty or meat sauce or taco by adding lots of chopped vegetables (onions, celery, spinach, etc.). Even though you pour or serve the same portion size, this time you’ve pumped up the fiber content of the serving.

5) Take as much time as you can to eat your food; at least 20 minutes. Okay, okay, I’m not talking about at EVERY meal (though that would be ideal), but at the very least, find ONE meal that you can enjoy at a relatively slower pace than normal.

6) Use smaller plates and glasses. Instead of filling 2 scoops of your ice cream into a cereal bowl, could you use a smaller bowl? Many of us have been conditioned to naturally fill our plates, so a smaller vessel will yield a smaller serving. Same thing with trading in your margarita glass that’s the size of a fish bowl with something that can only hold 6 to 8 oz.

7) Pace yourself with the slowest eater at the table. If you have a lot of business lunches and dinners to attend, or like to eat out socially, there’s always that person at the table who labors slowly over their meal (hint: that won’t be me). See if you can slow down to meet their pace.

8) At elaborate meals out, use the pick two rule outside of your main course.  Again, for those of you who eat out a lot socially or for work, instead of bread, wine, appetizers, main course, and desert, try to stick with one or two “play” foods rather than the four you might normally consume outside of the main course. So, wine+main course+desert or appetizer+main course. Just do the math right.

9) Designate an eating only room. Ideally this is the kitchen dining table or the main dining table; some room where the distractions are minimal. Plus, you won’t have to clean up frosting stains off your pillows.

10) Don’t deprive yourself of comfort foods. From early childhood, for better or worse, we’re all conditioned to feel a sense of comfort from certain foods that have been associated with feeling better/rewards. Like pizza after your team wins the game, or a lollipop at the doctor’s office after you’ve been vaccinated, or using ice cream to distract a whiny toddler meltdown.  I’m certainly not advocating that you bury your sorrows in a pint of Chunky Monkey, but depriving yourself of EVER having it once you begin your “diet” isn’t sensible either.

11) Allow a positive association with a non-comfort food, a healthier option, or even a non-food reward.  Let’s say you’ve just lost your first 5 lbs and have got another 40 to go. Reward your mini-milestone with something other than a food treat (buy a new pair of shoes or whatever form of “retail therapy” makes you happy, or a new set of smaller sized plates and glasses) or a healthier food treat (filet mignon instead of a burger, or a decadent chocolate truffle instead of an entire box). If we’re able to connect macaroni and cheese or cookies with happiness, our brains are probably capable of creating other positive associations.

12) Let your kid pick out a healthy treat in the grocery store.  This is one of my favorites. Every single time I check out of  the grocery store, my daughter is instantly drawn to the strategically placed candy.  While you are shopping, encourage her to pick a healthy treat, then let her look for the better/healthier choices that are there at the store too. Let her pick something like the pre-sliced apples or fruit salads, pre-packaged carrots, or single servings packets of animal crackers (I’ve even seen string cheese individually sold).  Then, at check out, remind her she’s made a good choice as far as a treat is concerned. You’re not always going to win, but you might, and the choices she makes might be better than the twizzlers or lollipops she’d normally hunt for.

13) Beware the health halo.  Just because they call it Fat Free or Lean Cereal or Healthy or Nature-Friendly or Organic or Raw or whatever doesn’t make it the best or healthiest choice for you. You can eat a pint of organic, cow-friendly  ice cream that is also perfectly fattening.

14) Be the “groceries gatekeeper.” If someone else (spouse, roommate, whatever) is responsible for grocery shopping for the house, he or she may not be picking the best choices for you. Even though you may write “fruits and vegetables” on the list, a non-dieter might hear “bananas and potatoes” rather than fruits and vegetables with more fiber (berries, apples, or leafy greens.) Similarly, they might not be as inclined as you might be to read labels. Therefore, things like salad dressing (reduced fat rather than regular), light, greek, or no-added sugar yogurt instead of the full fat versions, higher fiber breads and wraps instead of the highly processed white breads and tortillas might make it into your house, when you don’t intend for them to be there.  Read the labels at the store, shop the perimeters, and try to be the one who does the shopping, as much as possible if you can.

Finally, recognize that if you’re that person who has tried every trick or tool on the planet to shed the pounds gradually and NOTHING seems to work, it may be indicative of a more serious problem. Whether it’s thyroid or other metabolic issues, or if chronic fatigue or sleep issues make it difficult for you to make good choices during the day,  perhaps it’s something worth bringing up with your doctor.  Seek out a therapist if you think you might have an eating disorder or emotional issues tied to over eating, because even the best tools and tricks in the kitchen won’t help address habits that are embedded deep in the psyche. Just remember, there’s always the choice to make that first step, even if it’s a small one.

-Sumi Singh is a Personal Trainer in Austin, TX, an online diet coach, and the author of Stay at Home Strong. Her website is www.shailafitness.com and can be contacted for personalized diet coaching at sumi@shailafitness.com.  Her book is a program designed for post-partum weight loss and can be purchased at www.stayathomestrong.com

Re-Engineering Your Kitchen For Weight Loss is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

I’ve written several articles for The BrinkZone on weight training, fat loss, fitness modeling, bodybuilding programs, and various of motivational articles. The articles were meant to inspire and motivate both men and women to embrace the fitness lifestyle, and maintain the healthiest, leanest, strongest body possible no matter what age or excuse. And speaking of (good) excuses, stay-at-home, post-partum, and working moms are among one segment of the population that can benefit the most from simple, basic knowledge of weight training and fat loss advice that can help get them lean, strong, and healthy.

That’s why I’ve produced a book and DVD that addresses the many challenges that moms of all strides face when trying to achieve fat loss, and can help inspire you to lose that baby weight for good. It’s a great program that’s simple and effective.  Perhaps you’re a new mom or maybe a mommy of two or more, and you’re ready to drop a few pounds, and get back in your pre-pregnancy clothes. Or maybe you just want to get in the best shape of your life. This program is for you.

Congratulations on finally making you a priority! The journey to reach your fitness goals is not a selfish one because a stronger mom is a better mom. As a working mom, I don’t have endless hours to waste on time-consuming and exhausting workouts. That’s why I take out all the guesswork for you, so you can get right to work.

What is the Stay at Home Strong weight loss program?

• A 12-week post-pregnancy weight loss program to help you burn the baby fat and build lean sexy muscle.
• Ideal for post-partum moms, stay at home moms, or any mom short on time.
• A guided, step-by-step program that will help you achieve the same results that I did, and help you eliminate the many mommy excuses for being unable to achieve weight loss after your pregnancy.
• A complete program of exercise and nutrition requiring minimal, inexpensive equipment (or none at all) and little time investment.

What do you get with your purchase?

• Simple guidelines for strength training and cardiovascular activity,
• Pictures and videos for the exercises you can complete in the privacy of your own home,
• Pull-out fat loss meal programs and simple recipes for busy moms.
• Worksheets for goal-setting and compliance, as well as workout logs and a measurement tracker.

From start to finish, I take you through the many challenges that new moms and busy moms face when starting an exercise and post pregnancy weight loss program, and help you find ways to defeat the excuses and take on the challenges head on.

From fat loss meal programs to easy recipes, to dealing with birthday parties, holidays parties, travel, and other diet “saboteurs”, this book will compel you to make the choices that help you towards your goal.

What are YOU waiting for? Order your book and videos now for immediate download and start getting your body back today!

To get more information on the Stay At Home Strong program CLICK HERE Now.

-Sumi Singh is a Personal Trainer in Austin, TX, an online diet coach, and the author of Stay at Home Strong. She can be contacted for personalized diet coaching at sumi@shailafitness.com.

Post Pregnancy Weight Loss: Lose the Baby Fat For Good! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Part 1 of 3 on the deleterious effects of too much sitting 

Are you struggling to lose that extra flab and all those nasty calories that seem to be glued to your waistline? Do you ever wonder why, despite your hard training and dieting, you still have those annoying love handles? Then maybe you should try to implement the NEAT way to fat loss…

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NEAT – the ignored component of physical activity, metabolic regulation and total daily caloric expenditure

When it comes to fat loss, a key is to increase your energy expenditure. Therefore, the traditional prescription for fat loss has focused on exercise as a means of revving up your energy expenditure to burn off excess fat. While exercise (both cardio and weight lifting) is essential for fat loss, there is one other less known, albeit important, component of total daily energy expenditure that could be the missing link in your fat loss endeavor. Enter NEAT…

NEAT stands for non-exercise activity thermogenesis (or non-exercise activity energy expenditure). NEAT is the energy expenditure induced by non-exercise bodily movements in daily life, ie lifestyle embedded physical activity ¹.

The term “physical activity” represents the full spectrum of movement, with “exercise” being a subcategory representing the higher end of this spectrum ². The remainder that falls below the exercise threshold is “non-exercise physical activity”, and is illustrated in the graphic below.

Sedentary behaviors (typically in the contexts of television viewing, computer use, workplace sitting, and time spent commuting) are a new focus for research in the physical activity and health field.  As will be outlined below, emerging evidence is showing that there is a physiological distinction between too little exercise vs. too much sitting, i.e. exercise deficiency and sitting excess are each unique states with difference health consequences.

Sedentary behaviors include sitting during commuting, in the workplace and domestic environment, and during leisure time. Actually, the word “sedentary” comes from the Latin “sedere”, which means “to sit’. Sedentary behaviors, a.k.a inactivity, are defined by both posture (sitting or reclining) and low energy expenditure; they don’t elevate energy expenditure substantially above the resting level. In other words, sedentary “activities” incur an energy expenditure at the level close to 1 – 1.5 metabolic equivalent unit (METs). This can be compared to moderate/vigorous physical activity, or “exercise” such as brisk walking or running, which elevates energy expenditure 3-10 times resting metabolic rate, i.e. 3–10 METs.

Inactivity and sedentary behavior is characterized by sitting, reclining and lying down, which doesn’t elevate energy expenditure substantially above the resting level ³. In other words, sedentary activities incur an energy expenditure at the level close to 1 metabolic equivalent unit (METs) ⁴.

One MET is the energy cost of resting quietly, often defined as 1 cal/kg/hour (or 1 cal per 2.2 lb per hour) ⁴. To find out your “resting hourly burn rate”, ie how many calories you burn resting per hour, just divide your weight in lb by 2.2. For ex. a person weighing 150 lb will burn 68 cal (150 lb / 2.2), another person weighing 220 lb will burn 100 cal (220 lb / 2.2). It’s a rough estimate, but you get the idea.

Different activities elevate caloric expenditure over resting level as follows: ⁵

Sitting still                              3.7 %

Sitting while fidgeting         54 %

Standing still                         13 %

Standing while fidgeting    94 %

Slow strolling                         154 %

Fast strolling                         202 %

Even though standing still doesn’t markedly elevate caloric expenditure over sitting still, it is not considered to be a sedentary activity because muscle activity in the legs during standing is 2.5 times higher than during sitting ⁶. During standing, postural muscles (predominantly in the legs) are continually contracting to keep the body upright and maintain balance. This muscle activity during standing in turn stimulates an enzyme called muscle lipoprotein lipase (LPL) ⁷. LPL is the rate-limiting enzyme for the breakdown of fats circulating in the blood stream, and uptake of free fatty acids into muscle for use as energy (that is, fat burning) ^7-11. LPL has been studied heavily because this enzyme has a central role in several aspects of fat metabolism ^10,11. LPL also has a major influence on the partitioning of fatty acids between different tissues, plasma cholesterol metabolism and the subsequent downstream intracellular effects related to fat availability ^10,11. Thus, the differences between standing and sitting aren’t trivial. More on muscle LPL below.

NEAT vs. Sitting Time

Inactivity and non-exercise activity have gained growing attention because the proportion of time spent doing purposeful exercises usually make up only a fraction of the day, leaving much time for sedentary activities ⁷. Assuming 8 hours of sleep, we have 16 hours per day at our disposal. Studies that objectively measured physical activity show that people in the US on average spend about 8 hours daily, ie half of their waking time, being sedentary ¹². Those employed in sedentary occupations are sedentary for approximately 11 hours per day ¹³. The graphic below illustrates the major contexts for sedentary behavior and their distribution over a typical adult’s waking hours.

Therefore, it is no wonder that individual differences in light physical activity outside of intense exercise have greater influence on inactivity time than the time we spend exercising ⁶. This was confirmed in another study where some individuals participated in substantial amounts of intense exercise but otherwise had a relatively low overall daily physical activity energy expenditure ¹⁴. Thus, even when adhering to the exercise guidelines recommending at least 30 min/day of moderate-to-vigorous intensity activity at least 5 days per week ¹⁵, this does not automatically mean that people will not engage in excessive “baseline” sitting over the rest of the day. Because of this large amount of time we have at our disposal outside of formal exercise time, whether you spend most of your non-exercising time sitting, reclining, or standing and moving around, is a significant issue. this is underscored by the finding that 1 hour of daily physical exercise cannot compensate the negative effects of inactivity on insulin level and blood lipids if the rest of the day is spent sitting ¹⁶. And as  outlined below, too much inactive sitting can be what’s missing in your fat loss equation…

NEAT – small things add up fast in favor of fat gain or fat loss

This is true for both credit cards and energy expenditure. Energy expended during the day, outside of typical exercise (standing, fidgeting like movements while seated and while standing, ambulation) can vary by up to 2000 calories per day between individuals ^14,17,18, and thus may substantially contribute to the daily energy expenditure ^5,14,19. This can be explained by the very large variability between people in total inactivity times, ranging from 40 to 91%  ⁶.

It have been estimated that energy demands have dropped by over 400-500 cal/day due to occupational and domestic computerized environments, mechanization, and TV/media ²⁰. Therefore, even one hour of daily exercise might not be enough to achieve fat loss or fat gain prevention ^21,22.

What does research say about NEAT as a tool to keep body fat under control?

Caloric expenditure

To examine NEAT’s role in obesity, a study recruited 10 lean and 10 mildly obese sedentary people and measured their body postures and movements every half-second for 10 days ²³. The measurements were made using micro-sensors that subjects wore under their clothes and allowed body postures and movements to be accurately measured. It was found that obese individuals were seated 2.7 hours more per day than lean individuals. It was concluded that if obese individuals adopted the NEAT-enhanced behaviors of their lean peers, they might expend an additional 350 calories per day ²³, as illustrated in the following diagram:

This was confirmed in a later study which compared activity energy expenditure and daily activity patterns (using accelerometes) in lean and obese people ²⁴.  It was found that obese women sat 2.6 h more each day (12.7 h vs. 10.1), stood 2 h less (2.7 h vs. 4.7 h) and spent half as much time in moving around activity than lean women (2.6 h vs. 5.4 h) ²⁴. After controlling for differences in fat-free mass, the lean subjects expended 400 calories more per day than the less active and more sedentary obese subjects ²⁴.

It is interesting to note that this difference in magnitude of caloric expenditure between NEATers and non-NEATers is about the same as the formal exercise prescription dose that obese people are urged to adopt in order to induce a negative energy balance and fat loss (2500 cal/wk or 360 cal/day, corresponding to 75 min of brisk walking/d) ^25,26.  Thus, NEATing like standing/ambulating/fidgeting is of substantial importance for controlling body fat.

Interesting Statistics

Another study found that time spent watching TV is associated with risk of obesity and type 2 diabetes ²⁷. After adjusting for age, smoking, exercise levels and dietary factors, the following risk percentages were documented:

Each 2 hours/d increment in TV watching is associated with:

- 23% increase in obesity and a 14% increase in risk of diabetes.

Each 2 hours/d increment in sitting at work is associated with:

- 5% increase in obesity and a 7% increase in diabetes.

In contrast, standing or walking around at home (2 hr/d) is associated with:

- 9% reduced risk for obesity and a 12% reduced risk for diabetes.

Each 1 hour per day of brisk walking is associated with:

24% reduced risk for obesity and a 34% reduced risk for diabetes.

In this study population, it was estimated that 30% of new cases of obesity and 43% (95% CI, 32%-52%) of new cases of diabetes during a 6 year follow up could be prevented by adopting a relatively active lifestyle (less than 10 hr/wk of TV watching and at least 30 min/day of brisk walking) ²⁷. Many other studies support the association between sitting time and body fat gain ^22,28-35.

Waistline

Sedentary time is also deleteriously associated with a number of cardiovascular risk factors, including waist circumference, blood glucose, and blood fats ^36-38. Each 10% increase in sedentary time has been associated with a 1.2 inch (3.1cm) larger waist circumference ³⁶. The association between sedentary time and waist circumference is largely independent of exercise participation ³⁸. 

Not just total sitting time, but also breaks in sitting time are important. Compared to those who during the day have fewest breaks per hour of sitting, those with the most breaks per hour of sitting have been found to have 1.6 – 2.34 inches (4.1 – 5.95 cm) smaller waist circumferences ^65,66. Of importance to note is that a break could be as short as 1 min and doesn’t have to be intense type “exercise”, suggesting that regular breaks from sitting time can be easily implemented both during the working day and at home. A walk to the kitchen to take a sip of water, or walking around while drinking your coffee/tee, might be enough.

Thus, patterns of sedentary time accumulation are important in addition to total amount of sedentary time.

NEAT – your weapon against vacation and holiday fat gain

We all know about those lucky folks who magically appear to resist fat gain with overeating. These subjective observations have been confirmed in studies that documented a several-fold inter-individual variation in fat accumulation with overeating ^39-41. But what is it that makes those people resistant to fat gain?

To answer this question, a study was designed to find out if there is a component of energy expenditure that shows enough variability to account for the variability in resistance to fat gain during overfeeding ⁴². Non-obese volunteers were fed 1000 calories per day in excess of weight-maintenance requirements for 8 weeks. It was found that fat gain varied over 10-fold, ranging from a gain of only 0.8 lb (0.36 kg) to a gain of 9.3 lb (4.23 kg), and that it was changes in NEAT that accounted for this enormous difference. The maximum increase in NEAT was close to 700 kcal/day, and could be accounted for by an increase in strolling-equivalent activity by about 15 min/hour during waking hours.

It could be argued that it is the obese state that causes declines in NEAT. In order to find out whether differences in NEAT are a cause or consequence of obesity, the same obese subjects were put on a diet for 2 months which caused a weight loss of 17.6 lb (8 kg) ⁴². However, despite the weight loss, the original NEAT activities were maintained. This indicates that NEAT can be an inherent trait that causes some people to be more spontaneously active than others, and that a low NEAT that contributes to obesity.

The fact that NEAT is a mediator of the resistance to fat gain with overfeeding underscores its power. When people overeat, activation of NEAT dissipates a large part of the excess energy to preserve leanness, while failure to activate NEAT results in fat gain. Those who with overfeeding increase their NEAT the most, gain the least fat. Those who with overfeeding do not increase their NEAT gain the most fat and are predisposed to become obese.

Because the human genetic code has not changed during the past 50 years while obesity has become epidemic, obesity may in part be a consequence of enhanced responsiveness to environmental cues to be seated. But just because you don’t have an innate NEAT drive doesn’t mean you’re lost. Knowing the importance of NEAT as an anti-fat gain weapon, you can cognitively override your gravitation to the chair and consciously decide to simply move around more in your daily life.

Sitting – not just simply the opposite of exercising

Intuitively, sitting might be interpreted as the opposite of exercise, or lack of exercise. However, these two different behaviors each have unique effects, and therefore have to be treated separately. One molecular reason to maintain daily low-intensity ambulating activity is its importance for LDL regulation ⁸, as mentioned above. Muscle LPL activity is especially important since it is a prerequisite for the uptake and subsequent burning of fat that has been released from body fat stores.

What is intriguing is that sitting, low intensity ambulatory physical activity and high intensity exercise all have difference effects on muscle LPL activity ⁷.  For example, the reduction in muscle LPL activity in response to sitting is largely restricted to oxidative muscle fibers, while increases in LPL activity in response to exercise is mainly occurring in glycolytic muscle fibers. Further, the relative decreases in LPL activity seen in oxidative fibers following sitting are more than 4-fold greater than the increases observed in glycolytic fibers following vigorous exercise ^7,8,43.

It is notable that almost all of the LPL activity normally present in the capillaries (small blood vessels) of muscles is dependent upon low-intensity ambulatory activity ⁸. Muscle LPL activity decreases during inactivity and is very sensitive to non-fatiguing low intensity contractions, which rapidly reverse the sitting induced reduction in LPL activity ⁸. Thus, it is a misconception to think that ordinary spontaneous low-grade movements and weight-bearing activities in daily life are insufficient to elicit specific and notable physiological effects. This is underscored by the finding that those who do not exercise but have a high NEAT have a larger reduction in mortality risk thank those who partake in exercise but have low NEAT ⁴⁴. 

This means that an “active couch potato” might actually be healthier than a “lazy exerciser”. Further support for the independence of sitting and exercise habits in daily life is that the correlation between the two is very weak ³⁶, meaning that one doesn’t necessarily follow the other in the same direction. In other words, going to the gym is no excuse for spending the rest of your day on the couch.

Even if you exercise, sitting can be what’s halting your fat loss…

The fact that the mechanism linking LPL activity to sitting is distinct from that linking LPL activity to exercise, underscores the importance of viewing exercise and sitting as two separate factors influencing fat loss efforts and health outcomes. Too much sitting is not the same as too little exercise.

This is supported by evidence showing that sitting time increases the risk for expanded waistlines, obesity, insulin resistance, cardio-metabolic disturbances, cardiovascular disease and all-cause mortality independent of participation in exercise ^{21,22,27,34,36,45-62}.

For example, even among the most active people (those exercising at moderate-vigorous intensity for 60 min/day), spending 2- 4 hours per day in sedentary time (television viewing and screen-based entertainment) more than doubles the risk for obesity compared to spending less than 2 hours/day in sedentary pursuits ⁶³. Compared with people who watch television or videos or use a computer less than 1 h/d outside of work, the risk for the metabolic syndrome (which is a constellation of risk factors, including an expanded waistline) increases by 37 %, 70 % and 210 % for 2, 3 and 4 or more hours/day respectively, regardless of physical activity level ⁵².

Because the time spent in sedentary behaviors has been shown to be independent of exercise in population research, a recent study sought to examine within an individual whether exercise alters the time of muscular inactivity within his/her usual daily life ⁶⁴. Quadriceps and hamstring muscle activities (EMG recordings) and heart rate were measured during 6 days of normal daily living of ordinary people. Reported exercises varied from Nordic walking (aka. pole walking, a high intensity type of walking) to strength training and ball games lasting 30-150 min. It was found that muscular inactivity, defined individually below that measured during standing, comprised 72% of the day without exercise, and 68% of the day with exercise. This difference was not statistically significant (which means it could have occurred by chance). Also, duration of exercise was not correlated with inactivity time. The conclusion from this study is that exercise for fitness, regardless of its duration, does not decrease the inactivity time during normal daily life ⁶⁴. Bearing in mind the importance of muscle contractions for LPL activity, this is a very important finding.

Take Home

While diet composition has an important impact on nutrient partitioning and the relative amount of body fat that is gained or lost during overfeeding or dieting, the total energy expenditure in relation to you caloric intake is a determining factor in your fat loss efforts. However, sitting time is important not just because it robs you of energy expenditure opportunities. It also has unique molecular level effects that are separate from exercise. The finding that that exercising for fitness does not decrease the inactivity time during normal daily life ⁶⁴ underscores the importance of increasing daily non-exercise activities.

Evidence is rapidly mounting to suggest that long periods of sitting time have adverse metabolic and health consequences that are not necessarily compensated for by typical exercise. Therefore, if you are serious about losing fat, reducing sitting time, both at work and at home, is as important as is your exercise. Struggles with fat loss are not just about “too little exercise”. Mounting studies are showing the importance of “too much sitting”, and prominent researchers have stated that attacking physical inactivity and excessive sitting could help the battle against obesity ⁶². So don’t be surprised when you see public health media campaigns urging us to get our lazy butts off the chairs. Just remember where you read about it first!

Backed up by new scientific research, the new activity prescription for fat loss is “don’t just sit there – stand up and move, move around, more, more often”. Start turning circles in your typical fat loss routine and you might soon see those calories falling off your waistline. Injecting NEAT into your daily life outside the gym can really have a huge impact on your end-of-day caloric burn bottom line, your metabolism, resistance to fat gain, and ultimately on your fat loss success.

In part 2 of this series I will cover the detrimental effects of too much sitting on metabolic outcomes, cardiovascular disease risk factors, diabetes, cancer and mortality. In part 3 you will get lots of practical advice and tactics on how to inject non-exercise physical activity into your daily life and turn yourself into a fat burning NEAT-o-type machine. Stay tuned!

About Monica Mollica - www.trainergize.com

Trainergize is an informational and motivational resource, presenting the latest health related research findings to fitness geeks and health conscious people, in an easy to understand way.

While still under development, trainergize.com is committed to providing credible, objective, and reliable health information on a wide range of topics that impact your health and wellness and that of your family. The information is derived from scientific research studies published in top tier medical journals or presented at professional medical meetings.

Trainergize was developed and is maintained by Monica Mollica. Monica has a Bachelor and Master degree in Nutrition from the University of Stockholm / Karolinska Institue, Sweden, and has studied at renown Baylor University, TX. She is also an ISSA Certified Personal Trainer. Today Monica works as diet/nutrition/health counselor and health journalist, and is also a fitness model and web developer.

As a young athlete, Monica realized the importance of nutrition for maximal performance at an early age, and went for a major in Nutrition at the University of Stockholm. During her years at the University she was a regular contributor to the Swedish fitness and bodybuilding magazine BODY, and she has written a book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications. After having earned her Bachelor and Master degree in Nutrition, she completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, department of Health Human Performance and Recreation.

Having lost her father in an heart attack at an age of 49, she is specializing in cardiovascular health, and primordial and primary prevention. She is a strong advocate of early intervention in adolescence and young adulthood, and the importance of lifestyle habits for health promotion at all ages. Today, Monica is sharing her solid academic knowledge, real-life experience and passion, by offering diet/nutrition and exercise consultation services, and working as a health journalist and medical reporter on topics related to fitness, health and anti-aging. She is currently in the process of writing a book “Successful Aging – it’s your choice”, and developing the related website www.SuccessfulAging.me

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DHEA (dehydroepiandrosterone) is most known for being a pro-hormone which in the body gets converted to testosterone and estrogen. It is a long held view that DHEA exerts all its effects via conversion to testosterone and estrogen. However, recent studies show that DHEA also has several interesting non-hormonal actions…

DHEA 101

DHEA is produced mainly by the adrenal cortex, and is rapidly sulfated by sulfotransferases into DHEA-S. DHEA and its sulfated form DHEA-S is the most abundant steroid (pro)hormone circulating in the blood stream.[1] The sulfated from of DHEA has a longer half-life in the blood and its levels remain stable throughout the day, are not altered significantly by the menstrual cycle. When getting a blood test for DHEA, the fraction that is routinely measured is therefore DHEA-S. In response to metabolic demand, DHEA-S is rapidly hydrolyzed back to DHEA by sulfatases.

DHEA levels decrease approximately 80% between ages 25 and 75 year.[2, 3] This large decline in DHEA spurred research interest in the possibility that aging related DHEA deficiency may play a role in the deterioration of physiological and metabolic functions with aging, and in the development of chronic diseases.

How does DHEA really work?

No specific cellular nuclear receptor has been identified for DHEA.[4] Therefore, the actions of DHEA have traditionally been thought to be mediated via conversion to testosterone and estradiol, which in turn activate androgen and estrogen receptors and thereby elicits their effects.[5-7] However, emerging research is showing that the action of DHEA also involves multiple other receptors, and that DHEA and /or its oxygenated metabolites, such as epiandrosterone (EpiA) metabolites.[8, 9]

Increased NO production

One DHEA activated receptor, a cell surface (membrane-bound) receptor, that binds DHEA with high affinity has been identified in the endothelium (blood vessel wall), heart, liver, and kidney.[10-13] This receptor is coupled to eNOS (endothelial nitric oxide synthase) [10-12], the enzyme that activates the synthesis of NO (nitric oxide).[14] Endothelial cells exposed to varying concentrations of DHEA produced dose-dependent increased activation of eNOS and elevated nitrate levels (a bi-product of NO).[10, 12] This activation of eNOS by DHEA was not inhibited by the antagonists of the estrogen, androgen, or progesterone receptors, suggesting that eNOS activation by DHEA was through a very specific receptor for DHEA.[12] Support for this comes from another study demonstrating that DHEA supplementation 50 g/day for 2 months in healthy men aged 58+ years increased cGMP (platelet cyclic guanosine-monophosphate) concentrations, which is a marker of NO production.[15]

DHEA also activates an important vascular endothelial cell signaling pathway (ERK1/2) which plays an important role in vascular function.[16] This, combined with the DHEA induced elevation in NO production could explain the beneficial cardiovascular effects which have been seen in several DHEA supplementation studies in humans; such as improvement in vascular endothelial function, arterial stiffness and insulin sensitivity. [17-20]

The DHEA metabolite: 7-beta EpiA

Another exciting finding is that a 7-beta hydroxylated derivative of DHEA is physiologically active via a putative nuclear receptor.[21-23] It is especially notable that 7-beta-hydroxy-epiandrosterone (EpiA) inhibits COX-2 activity (the same enzyme that is targeted by NSAID) and markedly decreases production of the inflammatory prostaglanding PGE(2).[21, 22] 7-beta-EpiA also stimulates production of the anti-inflammatory prostaglandin PGJ(2).[22] Another study confirmed that 7-beta-EpiA stimulates the production of cell protective (cytoprotective) prostaglandins.[23]

These findings have important implications in health and disease. The inflammatory COX-2/PGE2 pathway is an important contributor to the development of cancer, and suppressing the COX-2/PGE2 pathway is a bona fide target for cancer chemoprevention and therapy.[24] In line with this, it has been speculated that a common factor of cancer and the metabolic syndrome may be low DHEA.[25] Thus, there is a good mechanistic basis for a potential beneficial effect of DHEA in inflammatory conditions and for cancer prevention.

Reduced production of pro-inflammatory cytokines and elevated IGF-1 action

Levels of inflammatory markers, such as serum amyloid protein A and C-reactive protein, are inversely correlated with DHEA-S levels, suggesting a role for DHEA in attenuating inordinate inflammatory responses.[26] In addition, DHEA inhibits production of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and TNF-alpha.[20, 27, 28]

As pro-inflammatory cytokines are known to induce IGF-1 resistance [29], by reducing their production DHEA indirectly may improve the responsiveness to IGF-1. DHEA supplementation also increases absolute levels of IGF-1 [30-35] and DHEA metabolites may stimulate aging cells in the anterior pituitary produce growth hormone (called somatotropes).[36] The stimulatory effect of DHEA on the GH/IGF-1 axis in humans is supported by several DHEA supplementation studies.[32-34, 37]

Reduced cortisol levels

DHEA supplementation lowers cortisol levels, even in young adults.[38-42] While it is still unknown exactly how DHEA exerts its anti-cortisol effect, several mechanisms have been proposed.[43] One speculation is that DHEA down regulates glucocorticoid receptors.[44, 45]

Chronically elevated cortisol levels stimulate development of obesity, diabetes, heart disease, mood disorders and memory impairments.[46-53] Administration of DHEA has been demonstrated to counteract the detrimental effects of cortisol in animals [54-56], and in humans, DHEA and cortisol produce opposing effects on the innate immune system; DHEA enhances while cortisol suppresses immunity.[57]

Lowering of cortisol levels with DHEA supplementation can indirectly provide additional benefits. Cortisol breaks down muscle tissue [58, 59], and suppresses testicular testosterone synthesis via multiple mechanisms. Notably, cortisol exerts a direct inhibitory action on testosterone producing Leydig cells in the testicles [60]. Cortisol also induces leptin resistance [53, 61] and thus may diminish leptin’s stimulatory effects on gonadotropin secretion of LH and FSH [62-64] and consequently diminish the secretion of sex hormones from testicles (testosterone) and the ovary (estrogen). Thus, by lowering cortisol levels, DHEA indirectly might confer several additional beneficial effects.

Improved Cortisol/DHEA ratio

DHEA, by reducing blood cortisol levels and elevating DHEA(S) levels, decreases the cortisol/DHEA ratio, which typically increases with age.[65, 66] This imbalance in the cortisol/DHEA ratio has been demonstrated to possibly contribute to several health derangements.

An increased cortisol:DHEAS ratios may contribute to reduced immunity following physical stress in the elderly[57], and may contribute to the development of cognitive impairment [67, 68] and stress-related psychiatric disorders.[69] The increased ratio of cortisol/DHEA-S is also positively associated with the metabolic syndrome and cancer/all-cause mortality.[70, 71] Thus, improvement of the cortisol/DHEA ratio with DHEA supplementation could help counteract age-related catabolism, metabolic dysfunction and prevent development of chronic disease.

Inhibition of the cortisol amplifier 11beta-HSD1

Cortisol levels in the blood is just one part of the picture. Obese humans and rodents have elevated levels of cortisol inside their fat cells (adipocytes), due to an increased activity of 11beta-HSD1 in adipose tissue.[46, 72-76]

11beta-HSD1 (11beta-hydroxysteroid dehydrogenase type 1) is an enzyme that elevates intracellular cortisol levels, irrespective of circulating cortisol levels in the blood, and thereby amplifies cortisol’s fat accumulating actions.[46, 72, 76]

Cause-effect evidence comes from rodent studies showing that transgenic mouse with elevated 11beta-HSD activity have increased cortisol levels in fat cells and develop obesity, expanded visceral (intra-abdominal) fat stores, high blood glucose (hyperglycaemia), blood lipid abnormalities (dyslipidaemia) and hypertension.[77-79] And conversely, pharmacological inhibition of 11beta-HSD1 effectively induces weight loss in obese mice and enhances insulin sensitivity and lowers blood glucose.[80-83]

An increased 11beta-HSD1 activity not promotes expansion of fat stores (especially in the abdominal region) but also contributes to metabolic derangement, which is why 11beta-HSD1 inhibition is an emerging therapeutic target for treatment of obesity, metabolic syndrome and type-2 diabetes.[46, 84-88] DHEA also inhibits 11beta-HSD1 activity in muscle cells, which could be an additional mechanism (on top of simply lowering blood cortisol levels) by which DHEA might prevent cortisol induced insulin resistance and muscle catabolism.[89]

Several studies have demonstrated that DHEA inhibits the activity of 11beta-HSD1 in fat cells from both rodents and humans [90-92], and thereby it counteracts cortisol’s fat storing effect [73, 74]. The inhibitory effect of DHEA on 11beta-HSD1 could be a contributing mechanism to the reduction in total body fat mass [93] and abdominal fat that has been seen with DHEA supplementation.[94]

Bottom Line

While many of the effects of DHEA are mediated via conversion to testosterone and estrogen and activation of the androgen and estrogen receptors, the studies outlined here clearly show that DHEA(S) is biologically active in its own right.

DHEA itself acts through specific cell surface receptors to increase eNOS activity and NO production, and contributes to intracellular signaling through activation of several intracellular messengers. DHEA also suppresses many of the detrimental effects of cortisol in muscle and fat tissue, and increases IGF-1 sensitivity and IGF-1 levels. Thus, it is time to re-evaluate the physiological role of DHEA and appreciate its multifaceted health promoting and potential fat loss actions.

For Additional DHEA info, more articles, videos, etc on DHEA on this site can be found HERE

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71.       Phillips, A.C., et al., Cortisol, DHEAS, their ratio and the metabolic syndrome: evidence from the Vietnam Experience Study. Eur J Endocrinol, 2010. 162(5): p. 919-23.

72.       Walker, B.R., Extra-adrenal regeneration of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1: physiological regulator and pharmacological target for energy partitioning. Proc Nutr Soc, 2007. 66(1): p. 1-8.

73.       Rask, E., et al., Tissue-specific dysregulation of cortisol metabolism in human obesity. J Clin Endocrinol Metab, 2001. 86(3): p. 1418-21.

74.       Rask, E., et al., Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-hydroxysteroid dehydrogenase type 1 activity. J Clin Endocrinol Metab, 2002. 87(7): p. 3330-6.

75.       Lindsay, R.S., et al., Subcutaneous adipose 11 beta-hydroxysteroid dehydrogenase type 1 activity and messenger ribonucleic acid levels are associated with adiposity and insulinemia in Pima Indians and Caucasians. J Clin Endocrinol Metab, 2003. 88(6): p. 2738-44.

76.       Wake, D.J., et al., Local and systemic impact of transcriptional up-regulation of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue in human obesity. J Clin Endocrinol Metab, 2003. 88(8): p. 3983-8.

77.       Agarwal, A.K., Cortisol metabolism and visceral obesity: role of 11beta-hydroxysteroid dehydrogenase type I enzyme and reduced co-factor NADPH. Endocr Res, 2003. 29(4): p. 411-8.

78.       Masuzaki, H., et al., A transgenic model of visceral obesity and the metabolic syndrome. Science, 2001. 294(5549): p. 2166-70.

79.       Masuzaki, H., et al., Transgenic amplification of glucocorticoid action in adipose tissue causes high blood pressure in mice. J Clin Invest, 2003. 112(1): p. 83-90.

80.       Hermanowski-Vosatka, A., et al., 11beta-HSD1 inhibition ameliorates metabolic syndrome and prevents progression of atherosclerosis in mice. J Exp Med, 2005. 202(4): p. 517-27.

81.       Park, J.S., et al., Anti-diabetic and anti-adipogenic effects of a novel selective 11beta-hydroxysteroid dehydrogenase type 1 inhibitor in the diet-induced obese mice. Eur J Pharmacol, 2012. 691(1-3): p. 19-27.

82.       Alberts, P., et al., Selective inhibition of 11beta-hydroxysteroid dehydrogenase type 1 decreases blood glucose concentrations in hyperglycaemic mice. Diabetologia, 2002. 45(11): p. 1528-32.

83.       Alberts, P., et al., Selective inhibition of 11 beta-hydroxysteroid dehydrogenase type 1 improves hepatic insulin sensitivity in hyperglycemic mice strains. Endocrinology, 2003. 144(11): p. 4755-62.

84.       Anagnostis, P., et al., 11beta-Hydroxysteroid dehydrogenase type 1 inhibitors: novel agents for the treatment of metabolic syndrome and obesity-related disorders? Metabolism, 2013. 62(1): p. 21-33.

85.       Tomlinson, J.W., 11Beta-hydroxysteroid dehydrogenase type 1 in human disease: a novel therapeutic target. Minerva Endocrinol, 2005. 30(1): p. 37-46.

86.       Morton, N.M. and J.R. Seckl, 11beta-hydroxysteroid dehydrogenase type 1 and obesity. Front Horm Res, 2008. 36: p. 146-64.

87.       Joharapurkar, A., et al., 11beta-Hydroxysteroid dehydrogenase type 1: potential therapeutic target for metabolic syndrome. Pharmacol Rep, 2012. 64(5): p. 1055-65.

88.       Masuzaki, H. and J.S. Flier, Tissue-specific glucocorticoid reactivating enzyme, 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1)–a promising drug target for the treatment of metabolic syndrome. Curr Drug Targets Immune Endocr Metabol Disord, 2003. 3(4): p. 255-62.

89.       Whorwood, C.B., et al., Regulation of glucocorticoid receptor alpha and beta isoforms and type I 11beta-hydroxysteroid dehydrogenase expression in human skeletal muscle cells: a key role in the pathogenesis of insulin resistance? J Clin Endocrinol Metab, 2001. 86(5): p. 2296-308.

90.       Apostolova, G., et al., Dehydroepiandrosterone inhibits the amplification of glucocorticoid action in adipose tissue. Am J Physiol Endocrinol Metab, 2005. 288(5): p. E957-64.

91.       Tagawa, N., et al., Alternative mechanism for anti-obesity effect of dehydroepiandrosterone: possible contribution of 11beta-hydroxysteroid dehydrogenase type 1 inhibition in rodent adipose tissue. Steroids, 2011. 76(14): p. 1546-53.

92.       McNelis, J.C., et al., Dehydroepiandrosterone exerts antiglucocorticoid action on human preadipocyte proliferation, differentiation, and glucose uptake. Am J Physiol Endocrinol Metab, 2013. 305(9): p. E1134-44.

93.       Libe, R., et al., Effects of dehydroepiandrosterone (DHEA) supplementation on hormonal, metabolic and behavioral status in patients with hypoadrenalism. J Endocrinol Invest, 2004. 27(8): p. 736-41.

94.       Villareal, D.T. and J.O. Holloszy, Effect of DHEA on abdominal fat and insulin action in elderly women and men: a randomized controlled trial. JAMA, 2004. 292(18): p. 2243-8.

DHEA – does it have any beneficial non-hormonal effects? is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

How It All Started

It didn’t take much. He was tall and lanky; I was not. But at 5’2” and 100lbs, I was far from overweight. All he did was wrap his hand around my arm, and then do the same to his own. An alarm sounded in my head — but on the outside, I didn’t move a muscle. I knew exactly what he was doing: he wanted to see if I was bigger than he was. I turned away very calmly without a word and left the room.

The following day began as usual. I hung around my 13 year-old peers, giggled my way through class, and turned in assignments late. Then lunchtime rolled around and I simply sat there. “I’m just not hungry,” I told everyone. The truth was, that friend from yesterday was sitting too close for my comfort. I couldn’t let him see me eat.

And so began the beginning of my dark days. As the months rolled by, I continued to skip lunch. And as I began to drop weight off of my already-petite frame, the compliments started rolling in. You’re so pretty. You’re so skinny. How do I get a body like yours? I loved it. No – I relished it, and I craved more. My breakfasts soon consisted of a few quick bites of whatever was on the table, and dinner was cut in half. My stomach growled on a constant basis, but that only made me feel strong. I have the power to resist the food; I can do anything.

It wasn’t just the eating, of course. As the star of my school’s swim team, I was pressured to perform. I was also on the varsity cross-country team at the time and my days consisted of long distance running followed immediately by two hours of grueling swim workouts. To that, I added a daily regimen of 200 pushups and 500 sit-ups every evening. I felt so accomplished.

Fast forward to six months later, and I was sitting at 92lbs. I ran into a friend’s mother who hadn’t seen me in almost a year. She gasped in delight, cooing over how much more attractive I’d become. “You’d look better if you dropped just a little more weight,” she said. “Maybe another five pounds or so.”  My heart dropped. What I was doing was not enough. People were still not happy with me.

I think something went off in me that day, and I went just a little bit crazy. I cut my food even more, and my exercise regimen became obsessive. I worked my way up to 300 pushups and 5,000 sit-ups. I spent my Friday evenings peddling away for a full three hours on the bike instead of hanging out with my friends like I so often had done. After all, it was the perfect opportunity to burn more calories, right? I was a social butterfly no more. I stopped laughing, I stopped smiling, and my thoughts revolved exclusively around food and the next time I could exercise. I went from being a mediocre student with the occasional C’s to straight-A perfectionist. Everything had to be exactly the right way; everything had to be planned out in advance, practiced until flawless.

Later in the summer, my family went out for lunch. I was vehemently opposed to this idea – I hadn’t eaten out in months, and who knew what could happen? – but was forced against my will to sit and eat. I felt nauseated because I could feel the food sitting heavily in my stomach. I’m going to gain all that weight back, a voice screamed in my head. Once we returned home, I walked nonchalantly to the bathroom and quietly closed the door. I wasn’t even thinking. I bent over, stuck my finger down my throat, and promptly threw up. I blinked. Then I smiled to myself as I wiped my vomit-stained mouth. Well, that was too easy. And that’s when bulimia entered the picture.

I was shipped overseas a few weeks later to attend summer school. It was the first time I was away from home for an extended period of time. I took advantage of that opportunity, and in my unhealthy state of mind, I delighted at the fact that my eating would not be monitored. I plunged deeper into my anorexia as I stopped eating almost entirely, only wolfing down food every third day, only to throw it all back up. My hair fell out in clumps, and I had long since stopped menstruating by then. I ran for 90 minutes every day with no rest. I made no friends that summer. I returned home teetering just over 80lbs.

Summer of 2003. I may be smiling here, but inside I was crying out for help.

High School Years

9th grade was a transitional year for me. Entering the high school scene was challenging enough, and add to that my struggle with food. I continued in my extreme, obsessive, restrictive ways for a number of months, but then something happened.

My body was royally pissed off at me. I wanted to continue starving myself, but I just couldn’t do it anymore. What happened to my will power? Was I getting weak? I felt defeated as I slowly increased my exercise even more to compensate for the food I was inhaling. Although I was purging on an almost-daily basis, my face, my legs, my entire body started to fill out again as I slowly began to put the weight back on. I felt constantly bloated and the shame was never-ending.*

By 10th grade, I was no longer anorexic but the bulimia still loomed ominously overhead. I was back to a healthy weight of 103lbs. I couldn’t seem to go more than a few days without binging and purging. It was such a vicious cycle: the anxiety-ridden urge to inhale as much food as possible, the panic as I forced myself to throw up, the vowing to never let this happen again as I brushed my teeth and tried to get the smell of vomit off of myself, the hiding of the bloodshot eyes, the feeling that I’d failed… only to do it all over again. If I so much as laid eyes on a plate of crackers, I had to eat the entire thing. And then I’d purge. If I was offered a few Wheat Thins, the whole box would be devoured within an hour. And then I’d throw up.

I wanted to be anorexic again, I really did. I yearned for it. But my body had had enough, and the feeling of my stomach eating away at itself was no longer something I could ignore. The incredible rush I’d once experienced from not eating for more than 24 hours stopped coming. I felt like I’d failed myself because I couldn’t make myself stick-thin again. Although I’d stopped my daily ritual of pushups and sit-ups, I still exercised for months and months at a time without taking a day off.

Protein? Carb? Fat? I had no idea what they were at the time, and I had no interest in taking the time to learn. I thought it was a waste of time and that I’d be better off continuing my miserable ways. In my mind, there was no way out. I was trapped forever, and the rest of my life was going to be more of the same. Dissatisfaction with my body, and consequently, myself as a person. I was never going to be good enough.

When It All Changed

One day during my second semester of 12th grade, I stumbled upon Oxygen magazine. I know it’s cliché, but where else are you likely to find a flock of athletic, lean women? At first I fell for a lot of the typical hype out there: eat bee pollen, plié squats only, take X Y Z enzymes, these fat burners, and this specific protein powder. I combed through The Eat Clean Diet** as though it was the bible and sucked in every word. I’d come across something that I’d never heard of in my life: you can eat food and not feel guilty or get fat? You can exercise and actually enjoy it? I’d long since given up on the idea that that was feasible, so to read about women who were doing it – and doing it well – shook my entire world.

Almost overnight, my mindset switched from starve, run, binge, purge, starve, run, binge, purge to lift, eat, lift, eat.  I spent every minute of my free time devouring information on bodybuilding.com and other fitness websites. I designed my own training programs (poorly made at the time, mind you) and began to lift on a regular basis. I cut down on my cardio, increased my protein intake, and was no longer afraid to eat healthy fats. Oatmeal became a staple in my diet, as did brown rice, fruit, chicken, protein powder, fish oil, nuts, and vegetables.

I hired an online trainer the summer after I graduated from high school, and the bulk of those months was spent adding more valuable tools to my fitness toolbox. I learned about compound movements, proper technique, the importance of rest, and corrected many of my misconceptions about what constituted proper nutrition.

Since then, I’ve undergone two off-seasons to build muscle mass and have made some sizeable strength gains in the gym. While my journey hasn’t been necessarily smooth sailing, I can now say that I have been in recovery from my eating disorder for some time. There’s no guarantee that I won’t fall back to my previous ways. But every day I make a thousand and one decisions, and each time I choose to respect my body, I am winning. And as long as I continue to win more days than not, I think I’ll be all right.

Where I Am Now

Today, I’m the strongest that I’ve ever been, both in mind and in body. It’s been a long time since I’ve graduated from the Eat Clean Diet days. I’m no longer afraid to eat real food – heck, I’ll even enjoy an avocado cheeseburger with onion rings (my favorite) every once in a while. In terms of training, I’m currently aiming to bench 120, squat 200, and deadlift 225 in the next few months. I can do unassisted chin-ups, which is something that I’d never dreamed of being able to do. While I’m far from being the strongest girl you’ll come across, I think I’ve come pretty damn far.

Fitness has become my passion. Over the years – through the depression, the breakups, the uncertainty of my life, the drama – fitness has been the one thing that I could always count on. I’ve competed in the NPC bikini division (now nationally qualified), received my NSCA certification, attended a fitness entrepreneurship conference, and I’ve also become connected to a myriad of individuals in the fitness industry. My heart still races whenever I think about lifting later in the day. I read fitness blogs as I sip my coffee every morning. I get excited when people ask me about training and nutrition. I argue with others about the best tasting protein powder out there (Gaspari Myofusion milk chocolate, hands down). I keep a training log to keep track of my progress and aim to push myself just a little more each week. I understand the importance of rest and exercise it (get it?) on a regular basis. I practically live in my workout clothes. Perhaps most importantly, though, I’ve fully embraced my past now and I’m not afraid to speak out about it.

Placing 2nd in A class at the 2011 NPC Contra Costa in May. This one’s a real smile.

I can’t tell you with full certainty where my love for fitness is going to take me at this point. For now, I’m doing what I love to do and having fun. Isn’t that that the point? Do what makes you happy, and everything will fall into place. That’s how I try to live anyway.

The moral of the story here is three-fold. First, I want to reach out to others, share my story, and let people know that fit is hip. If you’re in a dark place, know that there is a way out. I’ve been through hell and back, and today I am thriving. You’re not alone. Second, if you suspect that someone you know may be struggling with an eating disorder, please reach out to him or her. Sometimes all it takes is one person to save a life. Have the courage to be that person. And third, lifting weights is certainly not just for men, and ladies, I promise you it won’t make you big. I’ve never felt so confident about my body, and that’s all thanks to the iron plates.

Notes:

* You may notice that I never mention receiving any kind of professional help – and that’s because I didn’t. At the time, I didn’t even know what an eating disorder was and it never occurred to me that I was a victim. Unfortunately, given the culture that I was living in, my behavior was not uncommon and so nobody called me out on it. Seeking help would have saved me years of turmoil and anguish. I urge you to find the strength to reach out to others who may be suffering; you just may save someone.

** As a starter book, I found this perfectly adequate. I’ve even given this as a gift to a friend who was interested in becoming involved in fitness. At this point, however, there are many parts of the book that I disagree with and hesitate to recommend it to those just starting out.

Stay tuned for part II of this article, which will cover the science behind eating disorders.

One week after my show. I should have chosen lighter dumbbells to hold for the shoot!

Bio

Sohee Lee is a National Strength and Conditioning Association (NSCA) certified personal trainer. She is currently studying Human Biology at Stanford University and will receive her Bachelor’s degree in June 2012. She loves to talk fitness, admires those who can push and pull heavy weights, and loves her protein. She is currently trailblazing her way into the fitness industry and will shake the entire world, so look out!

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To Hell and Back: My Battle with Anorexia is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Can women suffer for “Low T” as men do? This vid covers the issue all women need to know about this “male” hormone! For additional details, see Monica’s article on the importance of testosterone in women HERE.

Study mentioned in this vid:

Low testosterone levels predict all-cause mortality and cardiovascular events in women: a prospective cohort study in German primary care patients

Sievers C. et al

Eur J Endocrinol. 2010 Oct;163(4):699-708.

Abstract

OBJECTIVE:

Although associations between testosterone and cardiovascular (CV) morbidity in women have been proposed, no large prospective study has evaluated potential associations between testosterone and mortality in women. The objective was to determine whether baseline testosterone levels in women are associated with future overall or CV morbidity and mortality.
DESIGN:

Prospective cohort study with a 4.5-year follow-up period.

METHODS:

From a representative sample of German primary care practices, 2914 female patients between 18 and 75 years were analyzed for the main outcome measures: CV risk factors, CV diseases, and all-cause mortality.

RESULTS:

At baseline, the study population was aged 57.96±14.37 years with a mean body mass index of 26.71±5.17 kg/m(2). No predictive value of total testosterone for incident CV risk factors or CV diseases was observed in logistic regressions. Patients with total testosterone levels in the lowest quintile Q1, however, had a higher risk to die of any cause or to develop a CV event within the follow-up period compared to patients in the collapsed quintiles Q2-Q5 in crude and adjusted Cox regression models (all-cause mortality: Q2-Q5 versus Q1: crude hazard ratios (HR) 0.49, 95% confidence interval (CI) 0.33-0.74; adjusted HR 0.62, 95% CI 0.42-0.939; CV events: Q2-Q5 versus Q1: crude HR 0.54, 95% CI 0.38-0.77; adjusted HR 0.68, 95% CI 0.48-0.97). Kaplan-Meier curves revealed similar data.

CONCLUSIONS:

Low baseline testosterone in women is associated with increased all-cause mortality and incident CV events independent of traditional risk factors.

The Importance of Testosterone for Women! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

EDITORS NOTE: A recent video I (Will Brink) did HERE  also discusses the fact T is just as important women as it is for men, yet continues to be ignored by most women and the medical community at large. Monica’s excellent article below give the full details!

Testosterone is popularly known as the “male” hormone. While it is true that men have much higher levels of testosterone than women, and that testosterone contributes to secondary sex characteristics that physiologically distinguish men from women (increased muscle mass and facial/body hair), this does not mean that testosterone isn’t important in women.

In the same way that men need estrogen, aka the “female” hormone, for optimal health, women need testosterone for optimal health. This article will describe testosterone physiology in women and its importance for women’s health, and refute the two prevailing myths that “testosterone is un-physiological in women”, and that “there is no research or clinical experience supporting the use of testosterone therapy in women”…. you may be surprised…!

History behind common beliefs of testosterone in women

In the past, circulating testosterone in women was simply considered to be a by-product of ovarian estrogen production. Surprisingly, testosterone circulates in the blood stream in levels exceeding those of estradiol (the major estrogen) by 200-fold (see below), and it is thus the most abundant biologically active hormone in women. In fact, testosterone in measured in ng (nanogram) while estradiol is measured in pg (picogram) units (1 nanogram = 1000 picograms).

This simple fact refutes the old notion that testosterone is “foreign” or un-physiological in the female body. Despite this, a long-held belief is that androgen administration to women is “anti-physiologic”.[1] This myth primarily underpins the fear of the use of testosterone therapy for women today [2], and probably contributed to making estrogen the hormone of choice for “replacement therapy” in women.

Testosterone production and levels in women

In women testosterone is produced and secreted by the adrenals (25%) and the ovaries (25%), each approximately 50 mcg per day, with the remaining 50% being produced in peripheral cells from circulating DHEA and androstenedione.[3-6]

Total daily testosterone production rate in women is in the order of 0.1–0.8 mg [3, 7] while in men it is around 6.9 mg/d.[7] The table below shows reference ranges for testosterone in women, measured by mass spectrometry (the golden-standard hormone assay that has accuracy even at low steroid hormone levels).

Table 1:  Age-specific testosterone reference ranges in women.[8]

Now, compare these numbers with the reference ranges for estradiol (also measure by mass spectrometry): [9]

* Pre-menopausal women in follicular, mid-cycle, and luteal phases of cycle:

2.4 pg/mL, 3.1 pg/mL and 2.6 pg/mL, respectively;

* Post menopausal women:       0.5 pg/mL

As the numbers shows, the highest estradiol reference number for a cycling woman is 3.1 pg/mL or 310 pg/dL or 0.31 ng/dL (note the differences in measurement units). As indicated in the table, testosterone reference ranges span from 8 to 63 ng/dL. Thus in women, natural testosterone levels are 25 to 200 times higher than estradiol! Tell this to anybody who claims that testosterone is un-physiological in women!

Contrary to estradiol, as the table shows, there is no sudden drop in testosterone levels in women with natural menopause.[10, 11] The largest decrease in testosterone levels in women occurs the early reproductive years, with no change across the menopausal years (ages 45–54).[10]  It should be noted that even after natural menopause, the postmenopausal ovary is hormonally active, contributing significantly to the circulating pool of testosterone.[12] This is in contrast to the abrupt 20-50% drop in testosterone levels in women who undergo surgical removal of both ovaries (bi-lateral oophorectomy, more on that below).[10, 13-16]

In premenopausal women testosterone is at its lowest concentrations in the early follicular phase of the cycle (after menstrual flow has ended) and rises to a mid-cycle peak.[17] As in men, women have a circadian fluctuation in sex hormone levels, with testosterone levels being highest in the morning around 8am.[18] In both pre- and postmenopausal women testosterone levels are significantly lower 3pm when compared to 8am. In premenopausal women, the same circadian fluctuation is seen for estradiol (the main estrogen).[18]

In regards to reference ranges, the fluctuations in testosterone levels during the menstrual cycle and during the day are relatively small compared with the overall inter-individual variability, so reference ranges can be applied in general irrespective of the day in the menstrual cycle the blood draw was taken and its timing.[19] However, it should be remembered that reference ranges are just a reference and not an indication of an optimal level for an individual for strive for (which displays a significantly inter-individual variability). Because of inter-individual differences in androgen receptor sensitivity (which is seen in both men and women), [20-27] changes in testosterone levels (both relative and absolute) over time are more informative in predicting outcomes than actual levels.[28] Therefore, is advisable to do regular blood draws at around the same clock time, so that deviations (increases or decreases) can be reliably monitored. This applies to both men and women.

Physiological importance of testosterone in women

Evidence that testosterone is of physiological importance in women and potentially plays important roles in multiple organ systems and female physiology comes from the fact that in human tissues (both male and females) there is a wide distribution of androgen receptors throughout the body. Studies have indentified significant androgen receptor expression in both male and female non-reproductive tissues, including the brain, skeletal muscle, breast, bone, kidney, thyroid, colon, lung and adrenal glands.[29-33] There is also significant expression of the androgen receptor in female reproductive tissues including endometrium, ovary, uterus, fallopian tube and myometrium.[29, 34-36]

Further indications that testosterone is important for women’s health comes from studies showing that bilateral oophorectomy (surgical removal of both ovaries) is associated with higher risk of coronary heart disease, stroke, osteoporosis, Parkinson’s, dementia, cognitive impairment, depression and anxiety, and overall mortality. [37-43] While it has been suggested that this is due to estrogen deficiency (when performed in young women), its long-term negative consequence on heart disease risk factors is not completely ameliorated by estrogen use.[44] The observation that women with oophorectomy are at greater risk for heart disease than intact women points to testosterone deficiency as a major contributing factor rather estradiol deficiency.[45]

Further evidence on the importance of testosterone in women comes from studies that have given women estrogen therapy after removal of the ovaries. One study found that pre-menopausal women who underwent oophorectomy experienced a significant worsening of vasomotor symptoms (hot flashes, night sweats and sweating) and a decline in sexual functioning (desire, pleasure, discomfort and habit).[46] The increase in vasomotor symptoms and the decline in sexual functioning were mitigated by post-surgery estrogen replacement therapy, but symptoms did not return to pre-surgical levels.[46] Another study in post-menopausal women also found that the negative effect of oophorectomy cannot be corrected by estrogen replacement therapy.[47] Thus, estrogen alone cannot make up for the consequences of the drop in testosterone that follows removal of the ovaries. Studies of both the consequences of oophorectomy and the effects of testosterone replacement are consistent with an important role for androgens in female sexual function, well-being and health.[48] In an upcoming article I will cover other causes of testosterone deficiency in women.

History of use of testosterone therapy in women

Few people know that testosterone therapy was reported to effectively treat symptoms of the menopause as early as 1937.[49] In 1938 studies demonstrated that testosterone therapy effectively treats various gynecological and sexual disorders.[50, 51] The actions of testosterone propionate on the uterus and breast was actually reported in the first volume of the highly acclaimed medical journal The Lancet in 1938.[51]

1941 the beneficial effects of testosterone in ameliorating various gynecological disorders in women were further documented in a study of women in different gynecological groups.[52] It was found that testosterone therapy effectively alleviates dysmenorrhea, after-pains, premenstrual tension and breast pain, dysfunctional uterine bleeding, and menopausal symptoms.[52] Interestingly, the study author states “The use of androgenic hormones for the relief of varied functional gynecologic disorders has now been thoroughly accepted.”[52] That same year it was shown that androgens are synthesized in the female and are the precursors of estrogen biosynthesis.[53]

1943 it was suggested that testosterone nullify or modify the action of estrogens, suppress or decrease the production of estrogens by the ovary and inhibit proliferation in the endometrium.[54] It was further reported that testosterone is effective in treating premenstrual tension and breast pain, dysmenorrhea (pain during menstruation that interferes with daily activities), postpartum engorgement of the breasts (painful overfilling of the breasts with milk), menometrorrhagia (prolonged or excessive uterine bleeding that occurs irregularly and more frequently than normal), and certain types of the menopause syndrome.[54]

Several studies published in the 1940s confirmed that testosterone increases women’s sexual libido.[54-56]

One of these studies specifically reported the following general effects:[55]

(a) Enlargement of the clitoris. No patient found this to be unpleasant.

(b) Increased sexual drive even in older women. The fact that this can be found without a single exception, even when the male hormone is given by injections in sufficient amounts, shows that testosterone can be designated as an “infallible aphrodisiac”.

c) All testosterone treated women acknowledge a great feeling of wellbeing, more balanced moods, and clearer thinking; and some profess also a greater determination.

In regards to the psychological effects, the study author amusingly reported “…we might therefore speak of a “chemistry of the emotions” in order to express that the temperament is influenced by the chemical substance so long as the hormone is active. It would be interesting to go further into this side of hormone therapy, and to study how the feelings might be chemically controlled. Some of Freud’s theses would perhaps have to be modified.”[55] Later is was confirmed that physiological doses of testosterone may be used to advantage in the management of the menopause, sexual dysfunction and breast disease.[1] Thus, the myth that “there is no research or clinical experience supporting the use of testosterone therapy in women” is clearly false. In upcoming articles I will report on more recent studies on testosterone therapy in women of all ages.

Conclusion

Contrary to common belief, testosterone levels in women are naturally higher than estradiol by some 200-fold, and are thus not un-physiological for women. The ovaries in women of all ages are a significant source of testosterone. Even the postmenopausal ovary is an ongoing site of testosterone production, although the production of estradiol ceases.

Little known, testosterone therapy has been clinically used since the 1940s to treat menstrual problems, sexual dysfunction, and menopausal symptoms. Studies on women who have had their ovaries surgically removed further clearly show the importance of testosterone for women’s health and wellbeing.

In upcoming articles I will report and comment on recent studies of testosterone therapy in women of all ages, and its beneficial as well as potential side-effects. Stay tuned!

References:

1.            Greenblatt, R.B., The use of androgens in the menopause and other gynecic disorders. Obstet Gynecol Clin North Am, 1987. 14(1): p. 251-68.

2.            Davis, S.R., Androgen therapy in women, beyond libido. Climacteric, 2013. 16 Suppl 1: p. 18-24.

3.            Longcope, C., Adrenal and gonadal androgen secretion in normal females. Clin Endocrinol Metab, 1986. 15(2): p. 213-28.

4.            Labrie, F., et al., Endocrine and intracrine sources of androgens in women: inhibition of breast cancer and other roles of androgens and their precursor dehydroepiandrosterone. Endocr Rev, 2003. 24(2): p. 152-82.

5.            Labrie, F., Intracrinology. Mol Cell Endocrinol, 1991. 78(3): p. C113-8.

6.            Labrie, F., et al., Physiological changes in dehydroepiandrosterone are not reflected by serum levels of active androgens and estrogens but of their metabolites: intracrinology. J Clin Endocrinol Metab, 1997. 82(8): p. 2403-9.

7.            Horton, R., J. Shinsako, and P.H. Forsham, Testosterone Production and Metabolic Clearance Rates with Volumes of Distribution in Normal Adult Men and Women. Acta Endocrinol (Copenh), 1965. 48: p. 446-58.

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45.          Barrett-Connor, E., Menopause, atherosclerosis, and coronary artery disease. Curr Opin Pharmacol, 2013. 13(2): p. 186-91.

46.          Finch, A., et al., The impact of prophylactic salpingo-oophorectomy on menopausal symptoms and sexual function in women who carry a BRCA mutation. Gynecol Oncol, 2011. 121(1): p. 163-8.

47.          Celik, H., et al., The effect of hysterectomy and bilaterally salpingo-oophorectomy on sexual function in post-menopausal women. Maturitas, 2008. 61(4): p. 358-63.

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49.          Salmon, U.J., Effect of testosterone propionate upon gonadotropic hormone excretion and vaginal smears of human female castrate. . Exp Biol Med (Maywood), 1937. 37(3): p. 488–91.

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Testosterone In WOMEN – is it physiological and clinically important? is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Important Information For Those on Thryoid meds and or SSRI’s

Considering how many people are on thyroid meds and or SSRI’s, it’s surprising – especially in the case of thyroid medications – how much confusion exists in the medical community on how best to treat people with hypothyroid.

I find many people feel they are often in some sort of battle between themselves and their doctor as to what doses, types, etc of thyroid meds they need.

A book called “Thyroid Disorders” written by a Dr Gilbert Daniels, listed as Co- Director of the Thyroid Clinic at Mass General Hospital makes for a good reference guide. The book was published in 2006, so I am assuming he’s still there. The book is written for physicians, specifically for GPs/family physicians vs. specialists. Most of the information would be basic rehash for the people here that have already done a lot of research on the topic, and most of what he recommends is in line with the standard recommendations. Some of Dr. Daniels comments below on T4/T3  combination therapy was supported by recent studies that found people on a combo therapy much prefer it over a T4 mono therapy.

However, he makes a few salient points regarding optimizing therapy, which seems to be the major issue for most people. Unlike many ‘traditional’ docs out there, Dr Daniels seems fairly open minded. For those looking for a decent reference guide to tests, diagnoses, etc, it’s a good little book. It could also be helpful for when making your case that you are not happy with your current meds/dose, etc and the doc you are working with is resistant. For example, he states:

“Although thyroid function can be precisely, monitored, not all ‘optimally treated’ patients feel well. For example in one study in which patients were treated with increments of thyroid hormone, those whose T4 dose was increased by 25-50 mcg/d, resulting in a suppressed serum TSH, felt consistently better than those receiving the highest dose at which TSH could be maintained within the normal range. In another community population-based study, patients taking T4 felt psychologically less well than a matched control population.”

Possible explanations for the above findings he lists as:

o Some of these patients may have been subtly under treated. When hypothyroid patients remain symptomatic, the T4 dose should be increased until TSH reaches the lower normal range.

(Note, however, he’s clear to point out that an intact hyopthalamo-pituitary axis is necessary for TSH to reflect thyroid status appropriately and other measures such as free hormones and symptoms should be used in that situation in addition to TSH)

o The patients may have remained symptomatic because their symptoms were related to other disorders possibly associated with Hashimoto’s thyroiditis, such as depression.

o True physiological replacement of thyroid hormone may require both T4 and T3.

o Clinical deterioration after starting T4 therapy should raise the question of concomitant adrenal insufficiency, known as Schmidt’s syndrome.

For a ‘traditional’ endocrinologist I thought his comments above showed an open minded approach I wish more docs followed.

Additionally, and changing topics a bit here, but germane to the situation of many people, recent studies find that t3 augments the effects of SSRIs, even with treatment resistant MDD, so those on SSRIs not experiencing improvements may want to talk with their physician/therapist about adding a small amount of t3.

Recent t3 and SSRI studies of interest follow for those who enjoy reading study abstracts. Obviously, optimal thyroid levels are essential for weight management and general health. However, a well planned and science based nutrition and exercise program are just as important, if not more so. If in need of such a plan, check out Fat Loss Revealed.

Studies of interest:

1: J Clin Psychiatry. 2005 Aug;66(8):1038-42.

An open study of triiodothyronine augmentation of selective serotonin reuptake inhibitors in treatment-resistant major depressive disorder.

* Iosifescu DV,

* Nierenberg AA,

* Mischoulon D,

* Perlis RH,

* Papakostas GI,

* Ryan JL,

* Alpert JE,

* Fava M.

Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA. diosifescu@partners.org

OBJECTIVE: In an open trial, we investigated the efficacy of triiodothyronine (T(3)) adjuvant to selective serotonin reuptake inhibitors (SSRIs) in subjects with major depressive disorder (MDD) resistant to SSRI treatment. METHOD: Twenty subjects who met DSM-IV criteria for MDD (mean +/- SD age = 44.3 +/- 10.3 years; 55% [N = 11] women) and had failed to respond to a course of treatment of at least 8 weeks with an SSRI antidepressant were enrolled in a 4-week open-label augmentation treatment with T(3) 50 microg/day. Atypical and melancholic sub-types of MDD were diagnosed using Structured Clinical Interview for DSM-IV Axis I Disorders criteria. We administered the 17-item Hamilton Rating Scale for Depression (HAM-D-17) 4 times during the study (which was conducted between 2001 and 2003). RESULTS: During T(3) augmentation, the severity of depression decreased from an initial mean +/- SD HAM-D-17 score of 20.5 +/- 3.6 to a final HAM-D-17 score of 14.0 +/- 7.1 (p < .001). Seven subjects (35.0%) were treatment responders (HAM-D-17 reduction >or= 50%), and 6 subjects (30.0%) achieved clinical remission (final HAM-D-17 < .01) greater clinical improvement (final HAM-D-17 scores 6.6 +/- 1.8 vs. 16.4 +/- 4.5), and higher rates of treatment response (100% [5/5] vs. 13.3% [2/15]) and remission (80.0% [4/5] vs. 13.3% [2/15]), compared to subjects with nonatypical MDD. The 8 subjects with melancholic MDD experienced significantly (p < .05) greater depression severity at the end of the study compared to nonmelancholic MDD subjects (final HAM-D-17 scores = 18.3 +/- 6.6 vs. 11.1 +/- 6.1). CONCLUSION: Triiodothyronine augmentation of SSRIs may be a promising treatment strategy in SSRI-resistant MDD, particularly in subjects with the atypical MDD subtype.

_____________________

: J Affect Disord. 2006 Apr;91(2-3):211-5. Epub 2006 Feb 17.

T3 augmentation of SSRI resistant depression.

* Abraham G,

* Milev R,

* Stuart Lawson J.

Department of Psychiatry, University of Toronto, ON, Canada. gaby_Abraham@camh.net

PURPOSE OF STUDY: To investigate whether the addition of triiodothyronine (T3) helps relieve depressive symptoms in non-hypothyroid major depressive disorder patients who failed to respond to an adequate course of standard SSRI antidepressant treatments. METHODS: Patients who fulfilled the DSM-IV criteria for non-psychotic major depression, able to give informed consent, and failed to show satisfactory antidepressant response after a minimum of six weeks adequate treatment were recruited. To enter the study their Hamilton Depression (17-item HAMD) score had to be 18 or more, thyroid-stimulating hormone (TSH) value within the normal range, and a normal thyrotropin releasing hormone-stimulation test (TRH-ST). All patients continued taking the same SSRI which they had been taking before they entered the study. At the completion of TRH-SH they were all started on 25 microg of T3 and the dose was increased to 50 microg within a week when tolerated; they continued the combination of T3 and the SSRI for a minimum of three weeks. RESULTS: Twelve patients, comprising eight females and four males, entered the study. One female patient withdrew during the first week of side effects, eleven patients completed the trial. The patients ranged from 26 to 77 years of age, with the mean age for males and females being 52.3 and 45.1 years, respectively. Five patients were taking sertraline (mean dose = 130 mg/day) and 4 were taking citalopram (mean dose = 50 mg/day), two were on fluvoxamine (150 mg/day) and one patient was on 40 mg of paroxetine. The women took a mean daily dose of 40.6 microg of T3 for a mean duration of 3.75 weeks, while the men were on a mean daily dose of 43.8 mug of T3 for 3.5 weeks. T3 augmentation was associated with a statistically significant drop (p < .003) in the mean HAMD at end of the three weeks compared to baseline scores. Five patients (42%) showed >or=50% improvement on HAMD scores, with three achieving full remission (HAMD scores

___________________________

J Clin Psychiatry. 2001 Mar;62(3):169-73. Links

Triiodothyronine augmentation of selective serotonin reuptake inhibitors in posttraumatic stress disorder.

* Agid O,

* Shalev AY,

* Lerer B.

Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel. agid@hadassah.org.il

BACKGROUND: There is considerable comorbidity of major depression and posttraumatic stress disorder (PTSD), and antidepressants have been reported to be effective in treating PTSD. Addition of triiodothyronine (T3) to ongoing antidepressant treatment is considered an effective augmentation strategy in refractory depression. We report the effect of T3 augmentation of antidepressants in patients with PTSD. METHOD: T3 (25 microg/day) was added to treatment with a selective serotonin reuptake inhibitor (SSRI) (paroxetine or fluoxetine, 20 mg/day for at least 4 weeks and 40 mg/day for a further 4 weeks) of 5 patients who fulfilled DSM-IV criteria for PTSD but not for major depressive disorder (although all patients had significant depressive symptoms). The Clinician-Administered PTSD Scale, the 21-item Hamilton Rating Scale for Depression, and the Clinical Global Impressions-Severity of Illness scale were administered every 2 weeks, and self-assessments were performed with a 100 mm visual analog mood scale. RESULTS: In 4 of the 5 patients, partial clinical improvement was observed with SSRI treatment at a daily dose of 20 mg with little further improvement when the dose was raised to 40 mg/day. This improvement was substantially enhanced by the addition of T3. Improvement was most striking on the Hamilton Rating Scale for Depression. CONCLUSION: T3 augmentation of SSRI treatment may be of therapeutic benefit in patients with PTSD, particularly those with depressive symptoms. Larger samples and controlled studies are needed in order to confirm this observation.

____________________

Am J Psychiatry. 2006 Sep;163(9):1519-30;

Comment in:

Am J Psychiatry. 2006 Sep;163(9):1484-6.

A comparison of lithium and T(3) augmentation following two failed medication treatments for depression: a STAR*D report.

* Nierenberg AA,

* Fava M,

* Trivedi MH,

* Wisniewski SR,

* Thase ME,

* McGrath PJ,

* Alpert JE,

* Warden D,

* Luther JF,

* Niederehe G,

* Lebowitz B,

* Shores-Wilson K,

* Rush AJ.

Massachusetts General Hospital, 50 Staniford St., Boston, MA 02114, USA. anierenberg@partners.org

OBJECTIVE: More than 40% of patients with major depressive disorder do not achieve remission even after two optimally delivered trials of antidepressant medications. This study compared the effectiveness of lithium versus triiodothyronine (T(3)) augmentation as a third-step treatment for patients with major depressive disorder. METHOD: A total of 142 adult outpatients with nonpsychotic major depressive disorder who had not achieved remission or who were intolerant to an initial prospective treatment with citalopram and a second switch or augmentation trial were randomly assigned to augmentation with lithium (up to 900 mg/day; N=69) or with T(3) (up to 50 mug/day; N=73) for up to 14 weeks. The primary outcome measure was whether participants achieved remission, which was defined as a score < or =7 on the 17-item Hamilton Depression Rating Scale. RESULTS: After a mean of 9.6 weeks (SD=5.2) of treatment, remission rates were 15.9% with lithium augmentation and 24.7% with T(3) augmentation, although the difference between treatments was not statistically significant. Lithium was more frequently associated with side effects (p=0.045), and more participants in the lithium group left treatment because of side effects (23.2% versus 9.6%; p=0.027). CONCLUSIONS: Remission rates with lithium and T(3) augmentation for participants who experienced unsatisfactory results with two prior medication treatments were modest and did not differ significantly. The lower side effect burden and ease of use of T(3) augmentation suggest that it has slight advantages over lithium augmentation for depressed patients who have experienced several failed medication trials.

Useful Info For Those on Thyroid or SSRI’s is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Why Women Need Resistance Training!

Here we are, the year 2014, and it’s stunning to me that myths surrounding weight training and women still exist, and worse yet, it’s the same myths I was hearing a few decades ago! It seems I can dispel these myths ’til I’m blue in the face, and yet, they persist! In addition to the myths, it seems many women are simply unaware of the many benefits weight training – also called resistance training or strength training  – can impart. Some of those benefits are sex specific in fact, that is, they are specific to women.

The following review below from the “THE PHYSICIAN AND SPORTS MEDICINE”  covers the major myths, which are:

• Myth 1: Strength training causes women to become larger and heavier.
• Myth 2: Women should use different training methods than men.
• Myth 3: Women should avoid high-intensity or high-load training.

For commentary on those myths above, see the review below. In addition to covering the myths, the review does a fine job of listing the benefits for women, which are :

• Enhanced bone modeling to increase bone strength and reduce the risk of osteoporosis
• Stronger connective tissues to increase joint stability and help prevent injury
• Increased functional strength for sports and daily activity
• Increased lean body mass and decreased nonfunctional body fat
• Higher metabolic rate because of an increase in muscle and a decrease in fat
• Improved self-esteem and confidence

One benefit I think this report missed, is strength training reduces the risk of sarcopenia. Sarcopenia is an age related loss of muscle mass which negatively impacts health of men and women. However, because women have less muscle mass to begin with, they are at a greater risk of sarcopenia as they age. I highly recommend women reading this also read my article on sarcopenia and how to avoid and or treat it. Most women are aware of osteoporosis -as it’s been drilled into their head via the media – but know little of sarcopenia, which is arguably more important to women than osteoporosis!Without further delay, here is a great review on the importance of strength training for women with some old, yet enduring, myths debunked!

Strength Training for Women: Debunking Myths That Block Opportunity

William P. Ebben, MS, MSSW, CSCS; Randall L. Jensen, PhD
THE PHYSICIAN AND SPORTSMEDICINE – VOL 26 – NO. 5 – MAY

In Brief: Traditional gender roles and differences in absolute strength have resulted in misconceived approaches to strength training for women. Male physiology, more than hormones, explains men’s superior absolute strength. When other measures of strength are used, such as strength relative to cross-sectional area of muscle, the strength of men and women is nearly equal. Women who practice the same well-designed strength training programs as men benefit from bone and soft-tissue modeling, increased lean body mass, decreased fat, and enhanced self-confidence.

Although American women first began strength training for sports in the 1950s to improve their performance in track and field, they have traditionally participated in strength training less than men. Such exercise has not been considered feminine, and a lack of research and information regarding the effects of such training on women has made it a predominantly male activity. Women’s participation was particularly limited until 1972, when Title IX mandated equal access to educational programs—including athletics—for men and women in schools that receive federal funding. Since then, women’s sports participation has burgeoned, traditional gender roles have loosened, and strength training has grown in popularity among active women.

Nevertheless, the social stigma and lack of accurate information persist and feed misconceptions that keep women away from strength training or prevent them from training in optimal ways (see “Dispelling Misconceptions,” below). Though gender differences regarding absolute strength exist, women are as able as men to develop strength relative to total muscle mass. Consequently, women should strength train in the same ways as men, using the same program design, exercises, intensities, and volumes, relative to their body size and level of strength, so they can achieve the maximum physiologic and psychological benefits.

Gender Stereotypes

Our culture has traditionally viewed strength as a masculine trait and promoted a small, frail body as feminine. Consequently, girls have been discouraged from participating in gross-motor-skill activities and strength development. Such sex role stereotypes, formed early in childhood, can dictate behavior and limit women’s and men’s ability to express their full humanity. This means that some women may have never achieved their potential for physical well-being, fitness, and athletic participation.

The advent of the women’s movement in the 1970s allowed many women to overcome such traditional socialization and participate more freely in sports and strength training. However, change occurs slowly, and physical strength and strength training are still not as common or accepted for women as they are for men.

A Gender Gap in Strength?

Research (1,2) on male and female strength potential reveals that women possess about two thirds of the strength of men. However, the measurement of strength in absolute terms fosters misconceptions about the strength of women, how women see themselves, and the way they exercise.

What causes this strength difference? Are there ways to conceptualize strength that affirm women’s potential and encourage their development?

The role of hormones. Hormones play a role in the development of absolute strength in men and women, but the exact influence is not clear. The androgens that come from the adrenal glands and ovaries are the hormones most likely to influence strength. The most important androgens for strength development are testosterone and androstenedione. The absolute androstenedione response to weight lifting is similar in females and males (3).

The role of testosterone in strength development is complex and significantly more variable than that of androstenedione. Though women on average have about one tenth the testosterone of men (4), the level of testosterone varies greatly among women and influences women’s strength development more than is typical in men (3). Women who have higher testosterone levels may have a greater potential for strength and power development than other women. An individual woman’s testosterone level fluctuates, so a woman who is near the upper limit of her testosterone threshold may have an advantage in developing strength compared with other women. Though hormones may influence strength development potential among women, they most likely do not account for significant male-female differences in absolute strength.

Physiologic factors. Physiologic differences such as size and body structure are more likely explanations for the average absolute strength differences between men and women. For example, the average American male is about 13 cm taller than the average female and about 18 kg heavier. Men average about 18 to 22 kg more lean body mass and 3 to 6 kg less fat than women. Men typically have a taller, wider frame that supports more muscle, as well as broader shoulders that provide a greater leverage advantage.

The Strength of Women

Strength, however, should not be viewed in absolute terms. The gender differences in absolute strength, for example, are not consistent for all muscle groups. Women possess about 40% to 60% of the upper-body strength and 70% to 75% of the lower-body strength of men (3). Men may have an advantage in neuromuscular response time that results in greater force production speed than women (5). However, the distribution of muscle fiber types—fast and slow twitch—is similar in the two sexes, and women are able to use a greater portion of stored elastic energy than men during activities in which muscle is prestretched, such as in the countermovement prior to jumping.

More significantly, if the amount of lean body mass is factored into the strength equation, the relative strength difference between men and women is less appreciable. Based on a strength-to-lean-body-mass ratio, women are about equal in strength to men, and when strength is calculated per cross-sectional area of muscle, no significant gender difference exists. For example, a 15 cm2 cross-sectional area of an arm flexor has about 19 kg of force for both women and men (6).

Measuring strength in this way suggests that muscle at the cellular level has a force development capability independent of sex and that women benefit from strength training at least as much as men. Hence men and women should follow strength training procedures that include periodization, variations in the resistance training program that are implemented over a specific time, and exercise performed at intensities and volumes suited to physical ability and level of strength conditioning. Ultimately, each athlete should be assessed as an individual, and training programs should meet individual needs and goals, rather than those based on preconceived ideas about gender.

The Benefits for Women

Women benefit from strength training in several ways (table 1).

Table 1. Strength Training Benefits for Women*

* Enhanced bone modeling to increase bone strength and reduce the risk of osteoporosis
* Stronger connective tissues to increase joint stability and help prevent injury
* Increased functional strength for sports and daily activity
* Increased lean body mass and decreased nonfunctional body fat
* Higher metabolic rate because of an increase in muscle and a decrease in fat
* Improved self-esteem and confidence

* A number of factors may reduce or eliminate these benefits, including the exclusive use of weight training machines, training with loads that are too light, and not progressing in resistance or intensity.

Bone and soft tissue. Women, more than men, need to meet the minimal essential strain required for bone modeling to occur and ultimately for reducing the risk of osteoporosis. Prevention of osteoporosis requires above-normal axial skeletal loading (7,8). The strain tolerance for skeletal bone is believed to be more than 10 times the typical load that humans bear in daily activities (9). Since bone modeling is proportional to the degree of overload (the amount of stress applied beyond the normal load), the greater the overload- within limits-the greater the amount of bone modeling. Bone modeling helps prevent fractures and insure against osteoporosis.

Cartilage, tendons, and ligaments also have minimal essential strain requirements. Optimal strength development requires loads and intensities that progressively increase the training stimulus or stress. Strong cartilage, tendons, and ligaments are essential for joint integrity, stability, and injury prevention.

Lean body mass and fat. Strength training also increases lean body mass and decreases fat; this results in less nonfunctional fat to carry and a greater proportion of lean body mass, which can provide functional strength. Compared to fat, muscle is metabolically active and increases metabolic rate, fat oxidation, and calorie consumption. Increased muscle mass and muscle cross-sectional area also correlate with increased strength. Participation in “functional” strength training exercises will develop functional strength and most likely improve performance, whether it is an increased ability to spike a volleyball or pick up a child.

Psychological well-being. Finally, studies (3) suggest that women who engage in strength training benefit from improved self-esteem. Female athletes appear to be able to balance strength and femininity; according to one survey, 94% of the participants reported that athletic participation did not lead them to feel less feminine. Strength training also appears to give women a sense of personal power, especially for women who have been raped or abused.

Such psychological benefits arise from the physiologic changes that occur as a result of strength training and from the process of encountering and mastering physical challenges. Thus, both the process and the outcome of strength training benefit women (3).

Strength Training Guidelines

Since well-designed strength training programs include exercises with free weights and dumbbells and exercises that use body weight resistance, both women and men should include these in their training, and women should train at the same intensities as men.

The use of strength training machines and abdominal exercises need not be discontinued, but emphasis should be placed on the use of free-weight exercises including foot-based lower-body exercises such as the lunge, diagonal lunge, walking lunge, step up, lateral step up, and squat. Women should also include upper-body exercises that employ multiple muscle groups such as the bench press, incline press, latissimus dorsi pull-downs, pull-ups, and back extensions. Finally, women who have developed a strength base should consider total-body exercises such as the push press, hang clean, power clean, clean and jerk, and snatch.

A training program should also stress multiplanar, multijoint, functional exercises because they develop intermuscular coordination, proprioception, and balance and result in strength that transfers to sports and daily activities. For example, the step-up exercise is superior to using the leg-extension machine because it offers functional strength for walking up a flight of stairs while carrying bags of groceries. For athletes who play foot-based sports such as basketball, the squat is superior to using the leg-press machine, since the squat is functionally more similar to the sport and requires greater balance and weight and body control in all three planes of motion.

Fostering Strength

Though sex role stereotypes still powerfully shape our culture and behavior, physical strength is no longer the sole domain of men. More and more women are claiming strength as their own through participation in sports and especially in strength training programs. Such participation helps to counter the stereotypes and fosters an appreciation of strength as desirable for women.
References

Dispelling Misconceptions

Recent studies counter several widely held beliefs that may limit the physiologic and psychological benefits of weight training for women.

Myth 1: Strength training causes women to become larger and heavier.

The truth is, strength training helps reduce body fat and increase lean weight (1). These changes may result in a slight increase in overall weight, since lean body mass weighs more than fat. However, strength training results in significant increases in strength, no change or a decrease in lower-body girths, and a very small increase in upper-extremity girth. Only women with a genetic predisposition for hypertrophy who participate in high-volume, high-intensity training will see substantial increases in limb circumference.

Myth 2: Women should use different training methods than men.

Women are often encouraged to use weight machines and slow, controlled movements out of a fear that using free weights, manual resistance, explosiveness (high velocity, low force), or exercises that use body weight as resistance will cause injury.

In fact, no evidence suggests that women are more likely to be injured during strength training than men. Proper exercise instruction and technique are necessary to reduce the risk of injuries for both men and women. All strength training participants should follow a program that gradually increases the intensity and load.

Furthermore, sport-specific exercise should closely mimic the biomechanics and velocity of the sport for which an athlete is training (2). The best way to achieve this is to use closed-kinetic-chain exercise that involves multiple joints and muscle groups and the ranges of motion specific to the sport. For example, the push press—rather than triceps kickbacks—offers a superior arm extension training stimulus for improving the ability to throw the shot put in track and field.

Myth 3: Women should avoid high-intensity or high-load training.

Women are typically encouraged to use limited resistance, such as light dumbbells, in their strength exercises. Often such light training loads are substantially below those necessary for physiologic adaptations and certainly less than those commonly used by men.

Most women are able to train at higher volumes and intensities than previously believed. In fact, women need to train at intensities high enough to cause adaptation in bone, muscle, cartilage, ligaments, and tendons. When exercise intensity provides insufficient stimulus, physiologic benefits may be minimal (3). To gain maximum benefit from strength training, women should occasionally perform their exercises at or near the repetition maximum for each exercise.

The Brink Bottom Line: If women don’t weight train, they are making a mistake….

Women And Weight Training: Debunking The Myths is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

INTRO: I remember well when Jenny was a new member  to the Fat Loss Revealed forums. She was in need of a serious revamp of her approach to  nutrition and exercise  to get the results she wanted. Like so many, she was confused and overwhelmed by all the conflicting and terrible information out there. What I didn’t know at the time was she had been dealing with eating disorders which obviously compounded her ability to get on the right track for her health, well-being and personal fitness goals. Regular writer for BrinkZone,  long time member of both the Fat Loss Revealed and Body Building Revealed forums, trainer, and owner of shailafitness.com, Sumi Singh does a Q&A with Jenny on how she finally broke threw the barriers, which I think everyone will find inspiring, regardless of where you are in your personal health/fitness journey. Jenny shows that with the right info, hard work, commitment to change, it can be done; be it fat loss, improved health, etc.

Excerpt  from “Overcoming Disordered Eating: A Personal Story”

Sumi: What was your first sign to yourself, that something wasn’t right?

Jenny: When you are so hungry and yet so afraid of people seeing you eat—for fear they’ll judge you— that you feel it necessary to sneak food and inhale it while hidden in a bathroom or closet…it’s a pretty strong indication something is not right.

Sumi: I understand you went through several phases; first anorexia, then bulimia. Or was it a mix of both?

Jenny in her various phases now fit and healthy!

Jenny: It was a mix over the years. I started by skipping meals and going long periods having only eaten a very small amount. That can really only be sustained short-term because people start noticing and the last thing I wanted was for someone to nag me about how I needed to eat moreAlso, you get really hungry eventually you binge because, well, you’re hungry. So that’s when the purging started because I realized I could eat and appease those people saying I needed to eat and the food didn’t really ‘count’ since it wouldn’t be staying down there for long. To me, that was balance—don’t eat around certain people, then eat and purge when you’re around others.I also exercised quite a bit; I grew up roller skating and I bought VHS tapes and did them at home. Cher’s first step aerobics VHS was my jam and I did it so much that I had it memorized (I could probably do it today with my eyes closed).

Sumi: When did you realize that you needed help? Who helped you? What steps did you take?

Jenny: This all continued on and off for around 9 years. I did go months at a time without purging, but disordered eating (skipping meals, hiding food, starving, and bingeing) was still very much a part of me for 9 years.Then I met the man that would later become my husband and he was accepting and loving and even though I thought I had hid my ED well (I had hid it from everyone else), he knew and he told me it wasn’t necessary and I believed him. I felt safe being me. I’m oversimplifying it, but really at that time, I thought that because he loved me, I could just be me and I’d be fine. I didn’t fear eating in front of him, so I ate. Unfortunately, I didn’t know how to eat properly; we were poor growing up, so all I knew was soda, fast food, spaghetti noodles with butter, comfort foods, etc. So what do you think happened? I got fat, that’s what happened. I basically swapped one extreme for the other.

It didn’t happen overnight, but little by little over the years I piled on the fat. I was overfat and feeling helpless—that was me. I could say that because I had stopped purging and I was now fat—which is what most consider to be the opposite of someone with an ED—that I was recovered from my ED, but I would be lying, right? Because overeating to the point of becoming overfat is still a form of disordered eating, isn’t it? Anyway, I didn’t want to go back to what I had done before, because I didn’t want to end up in the same place I started…

Meanwhile my husband was applying for a new career and we had started doing a lot of research about it and I ended up on some forums intended for those applying for this particular field. The application process required that you pass a physical agility test and there was this one guy on the forums that was super helpful to everyone and kept answering people’s questions on how to prepare for such a test.

That man was Will Brink. He was so knowledgeable on fat loss and fitness, so I started researching Will and found his Fat Loss Revealed e-book and forums. I bought his book in 2009 and I would say that’s when my real life-changing journey started.

I dove into the e-book and forums and started reading as much as possible, trying to learn how to lose fat and be healthy. At first it was like reading a foreign language, but I was determined and the moderators on the forum were so knowledgeable, helpful and patient…boy, were they patient. I asked anything and everything and if I didn’t understand, I would ask for clarification.

FULL INTERVIEW CLICK HERE

Overcoming Disordered Eating: The Jenny Goodwin Story is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness