The Moderation Epidemic

One of the biggest problems with attempting to do ‘everything in moderation’ is that as soon as you’re successful, the one thing that you’ll no longer be doing in moderation is – you guessed it – moderation.

In any case, they say that too much of anything is bad, and it’s hard to disagree with that statement. I mean, it is too much after all, and too much is bad. Which is a bit like saying bad is bad…because it’s bad!

But what does it mean to say that a person is consuming ‘too much’ of the sugary calories for instance? How are you really supposed to know when you’ve had enough of those pesky little critters?

The answer to this puzzle becomes more perplexing once you look a bit closer at the metabolic factors which come into play, regarding energy expenditure and the burning of calories, and the ways that impacts upon weight gain and weight loss.

“It is concluded that carbohydrate restriction plays an important role in mediating the fall in resting metabolic rate during hypocaloric feeding. This effect may, at least in part, be related to changes in circulating triiodothyronine [T3 active thyroid hormone] levels. Incorporation of carbohydrate in diet regimens may, therefore, minimize the thermic adaptation to weight loss.”

What if you were to find out that the reason why it’s difficult to avoid weight gain – or lose excess weight already acquired – has little to do with lack of moderation, and everything to do with the way stress (and things resulting from it) interferes with thyroid energy metabolism.

“The endocrine system, by modulation of anabolic and catabolic processes, plays a major role in the physiological adaptation to exercise training…four weeks of moderate aerobic training three times per week, significantly elevated the levels of stress hormones…The findings of this study also show that the increase of lactate at the end of exercise can elevate levels of cortisol during recovery…”

What if you found out that overdoing the moderation – as opposed to being a glutton – is something which can set in motion the conditions which can then lead to excessive weight gain.

What if you found out that you were exercising too much, and not eating enough.

The thing is, it’s not really as simple as just being a question of ‘how many calories you have consumed’, because numerous stress related factors come into play to determine your particular metabolic rate, and your metabolic rate directly impacts upon the number of calories required to gain fat. And not all food is made equal, so what you are eating, not just how much, can make all the difference.

Regardless, insufficient intake of calories can often be more stressful than excessive consumption, and (contrary to popular belief) it’s quite common for people to underestimate their caloric requirements, and overestimate their intake. Sugar restriction or famine reduces thyroid energy metabolism and encourages the stress metabolism to kick in. If you suppress thyroid metabolism enough, not only can you begin to gain fat with far less food consumption, you can start to have all sorts of health issues.

Exposure to chronic stress of any kind makes a person more susceptible to rising levels of a number of stress substances – such as cortisol, adrenalin, serotonin, estrogen, nitric oxide and lactic acid – produced in the body as part of an overall stress defensive process, interfering with and suppressing metabolism, reducing energy requirments, and increasing the potential for fat accumulation.

“Restricting…increased the total cortisol output among the participants, consistent with previous research…This finding may seem unexpected, as restricting caloric intake can trigger mechanisms to reduce energy expenditure…However, restricting caloric intake may be a biological stressor because one of the main functions of cortisol is to increase the availability of energy in the body.”

Stress increases the rate at which glycogen stores are depleted and as blood sugar supplies run low, cortisol and adrenalin are released in greater amounts to help provide alternative fuel (from fat and muscle tissue) for survival. Cortisol promotes fat production and storage, often interfering with thyroid metabolism and healthy weight loss.

“These results suggest that…greater exposure to cortisol observed among…men and women may have played a role in contributing to their greater abdominal fat depots.”

“Central fat distribution is related to greater psychological vulnerability to stress and cortisol reactivity.”

“…increased 11β-HSD1 expression in hypertrophic adipocytes is associated with reduced mitochondrial respiration and adiponectin synthesis… mitochondrial dysfunction in adipocytes might explain the reduced plasma adiponectin levels in obesity.”

One way the body deals with fuel insufficiency is via the release of fat out of storage into the bloodstream as an alternative to sugar. When free fatty acids are polyunsaturated they end up playing a big part in the promotion of stress, inflammation, metabolic suppression and insulin resistance, thereby encouraging obesity.

“Our findings suggest that adipose tissue LA [linoleic acid] concentration is strongly correlated with dietary LA intake…adipose tissue LA has increased by 136% over the last half century…At the same time…the United States has experienced substantial changes in disease prevalence…the prevalence of obesity…[has] increased.”

“The pivotal role of elevated plasma FFA levels as a cause for insulin resistance and as a pathogenetic factor in the development of T2DM has been established…elevated plasma FFA levels in obese subjects can produce a low grade inflammatory state which may contribute to the accelerated atherosclerosis and non-alcoholic fatty liver disease, conditions whose prevalence is several-fold increased in obesity.”

“…a high fat diet supplemented with oils high in LA [linoleic acid] leads to obesity and fatty liver. Other studies have also shown that dietary LA can cause adiposity in humans and lead to hyperglycemia as well as obesity…”

Increased exposure to polyunsaturated free fatty acids as a result of stress, low blood sugar and rising adrenalin, occurs around the same time levels of circulating amino acids begin to rise from cortisol breaking down muscle for fuel. Some of the amino acids are themselves inflammatory and metabolism interfering. Also the conversion of amino acids into sugar for fuel is a more expensive process than when sugar is readily available, and involves an increase in stress.

When stress is high, and more of the polyunsaturated fats (PUFAs) are circulating, another thing that happens is that tryptophan becomes increasingly likely to be converted into serotonin rather than niacin. Contrary to popular beliefs, serotonin interferes with energy metabolism and has been shown to be a powerful promoter of stress, inflammation and obesity.

“Obesity is characterized by the activation of the inflammatory process in metabolically active organs in the body. Typically this response leads to the elevation of pro-inflammatory cytokines, adipokines and other inflammatory makers…5-HT [serotonin] is an important mediator of inflammatory responses, including obesity…adipocytes have been determined to synthesize and secrete 5-HT…we demonstrate that feeding of HFD [high fat diet] results in…an increase in 5-HT production…leading to an inflammatory process.”

“Serotonin is synthesized from tryptophan by tryptophan hydroxylase…inhibition of peripheral serotonin synthesis…elevates BAT [brown adipose tissue] energy expenditure…this inhibition protects against obesity, non-alcoholic fatty liver disease (NAFLD) and insulin resistance.”

“In peripheral tissues, suppressing 5-HT signaling might represent a new target for anti-obesity treatment by increasing energy expenditure and improving insulin resistance…Systemic TPH1 inhibitors and a peripheral TPH1 inhibitor have already been patented for treating diabetes and obesity…”

Stress and interference with thyroid energy metabolism also promotes a rise in TSH [thyroid stimulating hormone], and TSH is well known to be a promoter of inflammation and stress (including high cortisol) in general. Increased TSH correlates with both insulin resistance and obesity.

When circulating PUFA levels increase and inflammation becomes more of a systemic issue, this interferes with the effectiveness of the thyroid hormones (T4 and T3), leading to further suppression of metabolism, more stress and inflammation, and the potential for obesity issues to worsen.

There are many angles from which one can view this type of scenario, and one which I believe is as crucial to the story as any other, relates to the negative impact that stress and reduced metabolic performance has on digestion, and vice versa.

Whenever digestion becomes sluggish, bacteria have a greater opportunity to feed and grow in number. This can end up promoting intestinal irritation and cause an increase in the release of endotoxin, serotonin, nitric oxide, estrogen and prolactin and various other inflammatory stress related substances.

“A slightly increased endotoxin load can induce a low-grade, chronic inflammation as a driving force for insulin resistance and altered lipometabolism in mice…Taken together, our results suggest that endotoxin-induced inflammation may have a pivotal role in obesity…”

“…strong evidence that BAT cells are sensitized to respond to the sympathetic nervous system and increase energy expenditure as a result of reduction in peripheral serotonin. These observations point the way forward for development of anti-obesity strategies targeting increased fat and glucose oxidation”

“…results indicate that increased expression of iNOS may play an important role in obesity-induced fasting hyperglycemia and suggest that iNOS may contribute to the defects in hepatic insulin signaling…”

Stress – and the suppression of metabolism – pretty quickly interferes with digestion and can impede barrier function, allowing for more toxic substances to pass through into the main system, placing a strain on the liver.

When the liver isn’t able to function optimally, bacterial and biochemical (or hormonal) issues, are more and more able to drive a systemic vicious circle of energy system interference, inflammation and fat accumulation. Fat tissue itself promotes estrogen production.

Sugar (in the context of a diet with enough protein, vitamins and minerals) improves the ability of the liver to excrete fat, but also to keep estrogen levels under control. Estrogen excess, especially when circulating levels of PUFA are high, promotes stress, inflammation and metabolic suppression, encouraging obesity.

“…oestrogen exposure is known to cause weight gain, primarily through thyroid inhibition and modulation of the hypothalamus.”

“Oestrone-fatty acid esters circulate in human blood in proportion to body fat, independently of gender. Plasma oestrone-fatty acid ester levels are associated with insulin sensitivity in men, independently of body fat. These findings may widen our perspective on the regulation of insulin action and control of body weight.”

Chronically high levels of the inflammatory anti-thyroid hormones can be dangerous regardless of issues relating to obesity. In fact, science is showing that continuously increased circulation of the stress substances can be more dangerous for a skinny person than for someone considered to be obese.

“An “obesity paradox” has been described, which reflects a relationship between obesity, compared with normal weight, and decreased mortality…demonstrated in diabetes, end‐stage renal disease, hypertension, heart failure, established coronary artery disease (CAD) and peripheral arterial disease…The improved survival of obese patients could be attributed to high metabolic reserves…a decrease in…oxidative stress and inflammation…”

Restrictive diets which sometimes lead to rapid weight loss, have the tendency to encourage inflammation and thyroid suppression, often eventually causing more weight to be gained than was lost, generally favouring fat deposition rather than muscle development.

“It is…well established that energy restriction and weight loss may cause a sustained suppression of the RMR [Resting Metabolic Rate]…the suppression of RMR may be important for understanding the high rate of weight regain in obese subjects after weight loss…The analysis showed that…formerly obese subjects had a 3–5% lower RMR than never-obese control subjects…”

Alternatively, any weight gained from the consumption of excess sugar calories has the potential to be pro-metabolic in the long run, protecting against PUFAs, lowering inflammation and helping with the recovery of thyroid and energy systems.

So called overeating – especially when it comes to the pro-thyroid metabolism enhancing foods – can assist in reducing levels of cortisol (as well as other stress related, obesogenic and catabolic substances) helping to promote improvement in muscle mass and quality, and increase metabolic rate.

Consuming more sugar (or carbohydrate in general) with enough protein and a few other nutrients, whilst avoiding too much fat (in particular PUFA), helps to protect against insulin resistance and blood sugar dysregulation, improves thyroid function, lowers cortisol, and in most cases eventually helps to reduce fat stores.

Sugar (by assisting thyroid function and cholesterol production), promotes the protective substances, such as pregnenolone, progesterone and testosterone, helping to counter the effects of stress, including the stress promoting effects of excess estrogen, protecting against obesity related issues. Low progesterone is also known to promote cortisol production.

“Negative correlations were observed between plasma progesterone levels and body weight, BMI, waist circumference, as well as subcutaneous adipocyte diameter. Plasma levels of 17-OH-progesterone, DHEA-S, androstenedione, testosterone and DHT were also negatively associated with body weight, BMI and waist circumference.”

“…progesterone binds both the progesterone receptor and the glucocorticoid receptor, for which it is an antagonist.

It isn’t always just a question of calories. To lose weight safely you need nutrients and fuel to keep stress low and metabolism high. Once your liver is able to store more glycogen, and bacterial issues have generally subsided, inflammation will lessen, and it possibly will no longer take as much food quantity to achieve (and maintain) good metabolic function. Healthy weight regulation does not come from eating less, but is rather the result of a well functioning metabolism.

The most important thing is to bring stress down, and skipping meals or limiting intake is far from being an effective stress reduction strategy, no matter how overweight a person might be.

“Skipping breakfast increases PPHG [postprandial hyperglycemia] after lunch and dinner in association with…impaired insulin response. This study shows a long-term influence of breakfast on glucose regulation that persists throughout the day.”

Calcium intake plays a major role in proper metabolic function and protection against obesity, and milk and some other dairy products are probably the most effective source.

“…an increase in dairy product intake was the main dietary factor associated with reductions in body weight in overweight adults…”

One problem with the idea of eating ‘excessive’ calories, is that the word excessive is often about as meaningful as the word moderation. Not meaningful at all. Whatever amount a person eats will be considered excessive if that person is gaining weight and becoming obese.

Someone on the other hand, who eats twice or three times that number of calories yet manages to stay the same weight, will probably not be judged as harshly. The only real way to obesity is via too much stress causing metabolic suppression. Quantity is mostly just a red herring.

“…chronic social stress causes…changes in BW [body weight], composition and endocrine measures that persist after repeated stress and recovery cycles and that may ultimately lead to metabolic disorders and obesity.”

There aren’t that many safe ways to use diet (or exercise for that matter) to lose weight rapidly. Rapid weight loss means excessive lipolysis, encouraging stress and energy metabolism suppression, increasing aging and disease risk, and often eventually making obesity issues worse. The ways that do work tend to take longer, and do so in a manner which keeps stress and free fatty acid (especially PUFA) exposure low, and improves metabolic rate, protecting health as the number one priority.

A diet avoiding PUFA as much as possible and generally limiting fat and difficult to digest grains, beans, seeds, legumes and under cooked vegetable matter, whilst eating smaller more regular meals of low fat milk and cheese and sugar from sweet fruit, fruit juice and white sugar, is one reasonable approach to lowering stress, inflammation and free fatty acid release, stabilizing blood sugar and improving overall metabolic function and weight regulation.

Some other things which have been shown to promote metabolic function and protect against stress, inflammation and obesity, include aspirin, niacinamide, cyproheptadine, activated charcoal, coconut oil, glycine, doxycycline, salt and sodium bicarb, bromocriptine, vitamin D, A, E, B1, B6 and biotin, methylene blue, coffee, caffeine, good quality sleep, and daylight and red light exposure.

There will always be a certain amount of fat released into the blood, however a well functioning metabolism limits free fatty acid exposure, reducing insulin resistance and stress hormone release, improving the ability of the cells to use sugar, and the liver and the muscles to gradually reduce excess fat stores whilst at rest. This is the optimal situation, the other is an emergency state. Obesity is not a disease of insufficient moderation, but rather a disease of improper information.

See More Here

Body Mass Index, Outcomes, and Mortality Following Cardiac Surgery in Ontario, Canada

Meta-analysis of resting metabolic rate in formerly obese subjects

The effects of four weeks aerobic training on saliva cortisol and testosterone in young healthy persons

Low calorie dieting increases cortisol.

Relationship between hair and salivary cortisol and pregnancy in women undergoing IVF

Neuroendocrine perturbations as a cause of insulin resistance.

Sex differences in corticotropin-releasing factor receptor signaling and trafficking: potential role in female vulnerability to stress-related psychopathology

11β-HSD1 reduces metabolic efficacy and adiponectin synthesis in hypertrophic adipocytes.

Vitamin A as a key regulator of obesity & its associated disorders: Evidences from an obese rat model

Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets.

Hair cortisol and adiposity in a population‐based sample of 2,527 men and women aged 54 to 87 years

45Obesity, Insulin Resistance and Free Fatty Acids

Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat.

Diet-induced obesity accelerates blood lactate accumulation of rats in response to incremental exercise to maximum.

Social stress and recovery: implications for body weight and body composition.

Acute psychological stress increases plasma levels of cortisol, prolactin and TSH.


Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

Stress-induced cortisol, mood, and fat distribution in men.

Pregnenolone protects mouse hippocampal (HT-22) cells against glutamate and amyloid beta protein toxicity.

An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice

Small differences in thyroid function may be important for body mass index and the occurrence of obesity in the population.

Activation of Pregnane X Receptor by Pregnenolone 16 α-carbonitrile Prevents High-Fat Diet-Induced Obesity in AKR/J Mice

Circulating progesterone and obesity in men.

Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice

Insulin resistance in obesity is associated with elevated basal lactate levels and diminished lactate appearance following intravenous glucose and insulin.

Plasma oestrone-fatty acid ester levels are correlated with body fat mass in humans.

Drug insight: selective agonists and antagonists of the glucocorticoid receptor.

Obesity is associated with increased serum TSH level, independent of thyroid function.

During rapid weight loss in obese children, reductions in TSH predict improvements in insulin sensitivity independent of changes in body weight or fat.

Circulating progesterone and obesity in men.

Increases in Nitric Oxide Concentrations Correlate Strongly with Body Fat in Obese Humans

A Role for iNOS in Fasting Hyperglycemia and Impaired Insulin Signaling in the Liver of Obese Diabetic Mice

Treatment with Cabergoline Is Associated with Weight Loss in Patients with Hyperprolactinemia

Increasing thyroid-stimulating hormone is associated with impaired glucose metabolism in euthyroid obese children and adolescents.

Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver

Reducing peripheral serotonin turns up the heat in brown fat

Increase in Adipose Tissue Linoleic Acid of US Adults in the Last Half Century

Reversal of Obesity- and Diet-Induced Insulin Resistance with Salicylates or Targeted Disruption of Ikkβ

Association between thyrotropin levels and insulin sensitivity in euthyroid obese adolescents.

Testosterone and obesity.

iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents

The Estrogen Hypothesis of Obesity


Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial.

Elevated thyroid stimulating hormone is associated with elevated cortisol in healthy young men and women

High Fat Diet Alters Lactation Outcomes: Possible Involvement of Inflammatory and Serotonergic Pathways

Blocking iNOS and endoplasmic reticulum stress synergistically improves insulin resistance in mice

Suppressed sympathetic outflow to skeletal muscle, muscle thermogenesis, and activity energy expenditure with calorie restriction



Image: Original Artist Unknown.

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