Thursday, 21 November 2013

Weight regain following weight loss

Biological mechanisms that promote weight regain following weight loss in obese humans.

Great paper here, summarizing the research on why maintaining weight loss is so difficult AND also the foolishness of calorie restriction.

This article discusses research on several factors that may contribute to weight regain following weight loss achieved through behavioural interventions, including adipose cellularity, endocrine function, energy metabolism, neural responsivity, and addiction-like neural mechanisms. All of these mechanisms are engaged prior to weight loss, suggesting that these so called "anti-starvation" mechanisms are activated via reductions in energy intake, rather than depletion of energy stores.

The bolded part is the key part of this paper. The author's are arguing that it is not weight loss per se that sets us up for weight regain, but rather it is the calorie restriction. I posted on another study earlier this year which also seemed to support this idea, here, in that post, we found that mice who lost weight by 40% calorie restriction had a dramatic increase in AgRP, while mice that were allowed to eat ad-lib on a new diet did not increase AgRP but still lost considerable weight. Whats funny is that the author of the above study makes no mention of the AgRP study I blogged about, so unwittingly he is on the right tracks. imo.

 The whole paper is golden so if you can get the full text its well worth a complete read. I tried and failed to paraphrase it, every sentence has useful information. So I just copy paste the beginning of the discussion and the conclusion...

Changes in adipose cellularity and addiction-like neural habituation result from chronic overconsumption and appear irreversible via behavioral weight loss [24,34,122,129]. Thus, these factors are not activated to prevent weight loss but serve to encourage preservation of highest sustained body weight, and may actually promote indefinite increases in energy storage. Alterations in endocrine function (e.g., decreases in leptin and increases in ghrelin), decreases in energy expenditure, and increases in neural responsivity to high-calorie food cues all occur within 24 h of caloric restriction (Table 1) [57,84,132]. 
Regardless of when these mechanisms are activated, each has the potential to exert a [neuro]biological influence that may reduce an obese or formerly obese individual's ability to maintain behavioral weight losses and promote weight regain at least to the individual's highest sustained lifetime weight. These influences also carry the expected weight regain promoting behavioral correlates. 
Weight-reduced vs. never-obese subjects report increased food craving [133], a decreased perception of amount eaten [134], decreased postprandial satiety [135] and an increased preference for calorically dense foods [136].With these additional biological influences encouraging the consumption and storage of energy, it is not surprising that weight regain following behavioral weight loss occurs at a faster rate than initial weight gain [135,137].
These mechanisms appear not to be part of a highly sensitive homeostatic feedback system designed to regulate body weight at any particular “set point,” but mechanisms either acquired via excess weight gain or enacted almost immediately via reduced caloric intake. Importantly, these mechanisms operate irrespective of the adequacy of energy stores. Thus, these mechanisms may be more accurately described as anti-weight loss mechanisms, rather than anti-starvation mechanisms per se.

We have presented evidence that the likelihood of weight regain in weight-suppressed obese and formerly obese individuals may be increased by a confluence of biological mechanisms, including adipose hyperplasia, increased metabolic efficiency, changes in neuroendocrine signaling (e.g., decreased satiety signaling), and changes in neural responsivity to both food cues (e.g., increased reward-related or decreased inhibitory anticipatory responsivity) and food intake (e.g., decreased consummatory reward through habituation to the rewarding aspects of palatable food). 
These biological pressures that may undermine weight loss efforts and promote weight regain are almost immediately enacted in obese individuals attempting even modest and healthy weight reduction. Further, these mechanisms operate invariably and appear to defend an individual's highest sustained body weight. Thus, it is the opinion of these authors that these mechanisms would be more accurately described as anti-weight loss mechanisms rather than anti-starvation mechanisms. Regardless, obese individuals face an extreme uphill battle in having to overcome powerful biological drives that appear insurmountable via behavioral interventions, illustrating the critical importance of obesity prevention efforts for normal and overweight individuals. This may be particularly pertinent to parents of overweight children, who are significantly more likely to become obese adults.
p.s. thanks to bill/caloriesproper for the full text.

EDIT -- Added the parts on adipose morphology and leptin

Excess weight gain typically leads to changes in body composition, including significant alterations in adipose cellularity. Although increases in body mass index (BMI) do not directly predict an absolute increase in body fat content [19], elevated body weight is generally associated with an increase in the diameter of fat cells (adipocyte hypertrophy), as well as greater amounts of fat stored within adipocytes [20,21]. Most literature points to adipocyte hypertrophy as the main feature of obesity; however, alterations in adipocyte number may also be important [22,23]. Upon reaching an upward critical limit in fat cell volume, enlarged adipocytes secrete paracrine factors that induce preadipocyte proliferation (hyperplasia) [24–26]. Thus, excess caloric intake* may lead to increases in fat cell size and subsequent increases in fat cell number [20,26,27].

Recent evidence suggests that this increase in fat cell number may occur in overweight individuals [28]. However, the preponderance of evidence suggests that hyperplasia occurs primarily in clinically severely obese individuals [27,29,30]. Thus, if hyperplasia is associated with weight regain, this effect may be relegated to weight regain following weight loss in [formerly] clinically severely obese individuals, for whom returning to a lean bodyweight through behavioral weight loss is exceedingly difficult [31].

With behavioral weight loss, adipocyte hypertrophy decreases; however, the hyperplasia remains [20,29,32–35]. Thus, weight loss dieting may reduce the size but not the number of fat cells. A lack of programmed cell death may be responsible for the failure of reductions in fat mass via nonsurgical means to reduce adipocyte number [20,33]. Therefore, relative to never-obese individuals, weight-suppressed [formerly] obese individuals (particularly clinically severely obese individuals) may be left with a significantly greater number of adipocytes, which cannot be reduced via behavioral weight loss [34]. See Table 1.

Liposuction is the only known treatment able to reduce adipocyte number, but carries high complication rates [36]. It is not yet definitively known whether hyperplasia encourages weight regain in weight-suppressed individuals. There is some evidence to suggest that the presence of smaller adipocytes may encourage weight regain by decreasing the overall rate of fat oxidation and increasing the retention of ingested fuel [37–41]. Normally, during times of energy deprivation, fat stores break down triglycerides into their individuals components, glycerol and free fatty acids [42], which generate energy for the cell. However, the rate of fat breakdown (lipolysis) appears to be related to adipocyte size and cellular surface area [43]; smaller cells exhibit lower rates of basal lipolysis [44]. Therefore, if size-reduced adipocytes are modified to break down less and store more fat, these cells may expand and promote further proliferation. Although still speculative, there is some evidence to suggest that these cells may be predisposed to reach a particular mean size, allowing them to store similar amounts of fat as previously formed adipocytes [25,34].

However, small adipocyte number may be sufficient to observe a clinically significant effect in only a percentage of obese (i.e., clinically severely obese) individuals.An additional line of evidence reports higher levels of insulin in newly size-reduced adipocytes [44,45]. Insulin, which is excreted from pancreatic beta cells in response to rising levels of glucose in the bloodstream, facilitates a preferential utilization of carbohydrates to meet the cell's energy requirements [40,46–48]. Further, insulin inhibits lipolysis [49] and stores triglycerides in adipocytes (lipogenesis) [50].

Interestingly, although insulin sensitivity seems to improve in weight reduced individuals, fat metabolism slows, potentially in an attempt to preserve energy stores [37,38,49,50]. As a result of these changes in carbohydrate and fat utilization, an abnormal accumulation of triglycerides may give rise to a higher net fat cell content and elevations in body weight [37,38,51–53]. Adipocyte size is also correlated with plasma leptin concentrations, which have been shown to affect weight loss maintenance [54]. Relative to control, formerly obese weight-suppressed participants were found to have reduced fat cell volume and serum leptin levels, despite almost identical body fat percentages [35].

Because smaller adipocytes in formerly obese individual smay be secreting less leptin following behavioral weight loss [28,35,37,55], an association between increased number of smaller adipocytes and leptin insufficiency has been proposed

Although leptin levels are not entirely depleted in weight-suppressed formerly obese individuals, their secretions are much more attenuated relative to lean subjects who undergo caloric restriction [35,55]. Thus, with reductions in leptin secretion, heightened appetite and excess food intake may lead to weight regain [28,54]. The potential role of leptin in weight regain is further discussed below.


Leptin levels are reduced within 24 h of energy restriction [57] and a number of studies report greater reductions of leptin than would be expected for given losses of adipose tissue [34,35,58]. It has been suggested that leptin's primary role is the prevention of starvation, rather than weight regulation per se, questioning the notion of “leptin resistance” [18]. Reductions in leptin levels appear to trigger a starvation defense response, despite the persistence of abundant fat stores [57]. Evidence suggests that there may be a threshold below which the “anti-starvation” action of leptin is enacted, and this threshold is proposed to increase concurrently with increases in adipose tissue [57].

Thus, weight loss dieting in obese individuals may lead to leptin depletion to sub-threshold levels, despite the persistence of relatively high levels of leptin. Sub-threshold leptin levels result in reductions in metabolic rate and physical activity [14], as well as increases in hunger and food intake [59]. Thus, behavioral weight loss and weight loss maintenance are accompanied by physiological attributes that resemble those of a leptin-deficient animal: lower energy expenditure, increased hunger, reduced thyroid metabolism, and diminished sympathetic nervous activity [60,61].

*I think that excess caloric intake quote is very ignorant of the author's. It is much more appropriately stated as excess storage of fat and/or insufficient mobilization of fat.

Tuesday, 12 November 2013

An easy way to increase testosterone......

During my research into steroids one of the more interesting studies that cropped up was this.....

Pharmacokinetics and dose finding of a potent aromatase inhibitor, aromasin (exemestane), in young males.

Aromasin is an aromatase inhibitor, it works by binding irreversibly to the aromatase enzyme, so that other steroids like testosterone cant bind to it. In this study young males were given 25mg per day ( which is the standard tablet size ) for 10 days.

At the end of the 10 days, total testosterone had increased ~60% but free testosterone ( that is, the testosterone that is actually free to bind the androgen receptor ) increased by 117%. The reason this works is because estrogen is reduced as a result of the aromatase blockage, and estrogen is the main negative feedback signal to the hypothalamus to decrease LH secretion. So with lower estrogen in the system, more LH is secreted and more testosterone is made. Its a double whammy aswell, because with aromatase blockage, less testosterone is lost in the conversion to estrogen.

Infact another recent report even suggested aromatase inhibitors may be of benefit to obese men who suffer from hypogonadism due to the excess estrogen that usually accompanies obesity.

Whether or not this increased testosterone will result in anabolic affects however is up for debate. However if you think your suffering from low testosterone, aromasin could be of some help. Aromasin is actually quite a safe drug, with minimal side affects, but it is slightly pricey.

Note in the first study, estrogen levels returned to normal 3-6 days after aromasin withdrawal, so the drug must be continuously taken to keep the increased levels of testosterone. Bear in mind also, estrogen is actually a very important hormone in men, lower is not necessarily better. Low estrogen will absolutely murder your sex drive and ability to get an erection, in a similar way low testosterone will.

Sunday, 10 November 2013

Insulin "turbocharges" conversion of testosterone to estrogen

This may be old news to many.....

So aromatase converts testosterone to estrogen, and aromatase activity is greatly increased by insulin, something of which we all seem to have too much of in our modern society. ( insulin that is )

Here is an interesting passage from this paper.....

The physical effects of illness and inflammation, and the psychological stress associated with concern about being loved and accepted by family and peers, compounded by work pressure, financial stress and the perceived urgency of daily living, all contribute to effectively increase corticotropin releasing hormone (CRH) Foster et al., 2009. The resultant pituitary adrenocorticotrophic hormone (ACTH) and corticosterone output stimulate the increased consumption of sweet and palatable carbohydrates (Dallman et al., 2007), including foods that contain 30% sucrose (like many breakfast cereals, cakes, biscuits, and confectionary), that stimulate a normal reactive insulin response.
Unfortunately, the increased insulin output,

  • upregulates P450 aromatase 6-fold (Samad, 2007),
  •  increases leptin output (Thomas et al., 2000; Falconnier et al.,
  • 2003; Manderson et al., 2003; Lindsay et al., 2004),
  •  increases estrogen-receptor-alpha number and activity (Kaaks, 2008),  
  • induces hypertriglyceridemia, sodium retention and hypertension (Biddinger and Kahn, 2006),
  •  increases subcutaneous fat deposition (Shin et al., 2007),
Further from the author.....

In summary, continuing exposure to stress, compensatory eating, xeno-oestrogens, the pill, pesticides, oestrogenic chemicals, fast foods, soft drinks and poor quality carbohydrate diets, cyclically amplify aromatase to TURBOCHARGE the production of even more oestradiol. . .until overweight becomes obesity, stress becomes depression, glucose intolerance becomes type two diabetes, benign prostate and breast changes turn into prostate cancer and breast cancer, and acceptable forgetfulness progresses toward Alzheimer’s disease.

In reference to the bolded part, the author recognizes that it is the carbohydrates in the diet that need to be scrutinized, not the dietary fats. Personally I think the cause of gyno in people taking high doses of steroids/androgens actually comes from the "bulking" aspect of their diet that generally involves extremely high amounts of calories/carbohydrates/refined carbohydrates. All the insulin that follows such a diet no doubt "turbochargers" aromastase to convert all that testosterone your injecting into estrogen.

There is also the link between increased levels of stress and increased carbohydrate consumption that has been reported many times before. To be honest, unless you are financially well off, modern life is almost 24/7 stress.

IF your still on the fence to the eternal chicken and egg question of what comes first, insulin hyper-secretion or insulin resistance, but still want to reduce your aromatase activity. You can do either one of two things, reduce your insulin resistance, or reduce your insulin secretion. ( or both obviously ). Reducing insulin resistance is not something that can be done in an obvious way, otherwise we'd have a cure for type 2 diabetes. HOWEVER, reducing your insulin secretion is easily done by reducing carbohydrates in your diet.

Tuesday, 5 November 2013

My experience with steroids

As mentioned previously, I finished a steroid cycle some weeks ago and I just want to make a small blog post on my experiences.

Originally I started taking testosterone ( 500mg 1x injection per week, rotating quads and glutes ) to help with my depression. Another reason I started testosterone is also because I badly wanted to try  Anavar which was reported to be especially good at reducing subcutaneous belly fat. I couldnt run the Anavar alone you see, because it would result in shutdown of testicular production of testosterone.

Anyway, after spending sometime researching the whole subject ( which was really fascinating ) I decided to get over my needle anxiety and start a cycle. Im no bodybuilder, I wasnt looking to gain huge amounts of muscle, just to deal with my depression and re-composition my body a bit. The first thing I would say is that the injections themselves are relatively painless. I used a 25gauge needle, and apart from the awkwardness of injecting into your own bum it was much easier than I thought. There can be some after pain, referred to as *pip* ( post injection pain ). I did get this on my first few shots, but as my skill injecting improved so did the pip. One tip is not to let the needle wiggle around when its in the muscle.

It took about 2 weeks before I started to notice changes in musculature and strength, however I noticed psychological changes within 48 hours. Suddenly I was EXTREMELY confident, much more assertive than I normally am, and would hold eye contact much more during conversations. Contrary to poplar belief, I did not experience any change in aggressiveness. One thing that testosterone clearly does is greatly increase your belief in yourself. Libido also increased. and my forehead and chest got extremely greasy.

Luckily I experienced only a very mild increase in acne, some people apparently really breakout badly with acne with high androgens. 6 weeks into the cycle I had gained only small amounts of muscle, my belly fat had gone down quite a bit which I was happy with ( thanks Anavar ), and my strength was up ALOT. But by far the best improvements were the psychological ones, the feeling of well-being was euphoric. Steroids make you feel like you can do *anything*.

At this point I made a big mistake and added Trenbolone. I dont know why, probably because I was still desperate to drop bodyfat plus so far I had experienced almost no negative side-effects from the testosterone and anavar. Trenbolone is notorious for its side-effects and I can say that is very true. I noticed immediately upon adding the Tren that I become short-tempered ( very unlike me ), but by far the worst thing was the insomnia, I was sleeping 3 hours per night and it was completely ruining me. One thing I noticed, which might be placebo, was that people seemed to be acting in a naturally more supplicating/timid way towards me while I was on the tren. I stopped going to the gym due to being completely fatigued all the time. And I was sweating badly constantly. I had to wait several weeks for it to clear form my system due to the long ester version.

After that, I increased the testosterone dosage to 750mg per week, then a few weeks later ended the cycle. I used HCG throughout cycle to avoid testicular atrophy. It is commonly advised to use an aromatase inhibitor during cycle to combat estrogen and gyno, HOWEVER I believe this is because most people running steroids are also running highly insulinogenic diets that promote hyperinsulinemia, and insulin is a strong activator of the aromatase enzyme. I spent alot of money on aromasin and found it to be a COMPLETE waste, because not once did I ever experience signs of high estrogen. ( I was still lowcarb during the cycle ). Infact the few times I did try taking the aromasin I immediately experienced signs of LOW estrogen, such as achy joints/spine and complete loss of libido.

Well, I am now 2 months since the end of my cycle, Ive lost pretty much all the muscle I had gained ( mostly because I stopped going to the gym ). however I do seem to have retained some of the strength gains. Yes, im going to run steroids again in the future, However I will stick to just testosterone, anavar, and dianabol. IF theres one thing I learnt its to keep side-effects to an absolute minimum.

I think the stigmatization surrounding steroids is completely overblown, sure they are open to abuse just like any drug. I find this especially amusing since just about EVERYONE in the sports and fitness industry is on steroids. ALL Olympic athletes are on these compounds, as most probably 99% of sports stars are. Even movie actors are taking these things in high doses just to look good for movies.  ( Thor, Bane, etc ).

Personally I predict a massive explosion of steroid use in the future, especially as we learn to control the negative side effects of them. People dont want to be just average, they want to be GREAT.

P.S. sorry for the dark tone this blog is taking, but I have warned people previously that this is my personal space.

Saturday, 2 November 2013

Fats reduce protein catabolism?

Just a quick update, I dont really have time to blog at the moment since I have alot going on in my real life. My father died in June and I have been suffering with pretty severe depression since then. It caused me to start steroids, mainly because testosterone is the best anti-depressant available to men. Anyway, ive come off them now, it was interesting and certainly helped me cope with the depression. I also managed to fall for a girl I apparently have no chance with, which has been a MAJOR headache. So yeh, my life is pretty fucked up at the moment.

Well, I dont want to discuss too much of my personal goings on here, I found this study today which seems to provide some answer to the strange paradoxical question, why would you lose muscle mass on a hypo-caloric diet despite consuming surplus protein? ( say 800 calories per day 150g protein ).

Hepatic amino acid-degrading enzyme expression is downregulated by natural and synthetic ligands of PPARĪ± in rats.

PPARalpha is activated by fats, including dietary fats, and according to this study PPARalpha down-regulates protein degradation. So in a strange way, eating fat may help with increasing or preserving muscle mass. I think this is a good explanation for as to why 2000 calories 150g protein 150g fat would be better for muscle mass than simply a 800 calorie diet with 150g protein.