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 – that’s right – 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’s ‘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 closely 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 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 you find it difficult to avoid weight gain – or lose excess weight already acquired – has little to do with a lack of moderation and everything to do with stress – and things resulting from it – interfering with 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 commonly sets in motion the conditions which lead to excessive weight gain.

The thing is it’s not really as simple as just being a question of ‘how many calories you have consumed’, because numerous factors – related to stress – come into play determining your particular metabolic rate, and your metabolic rate directly impacts upon the number of calories required to gain fat.

Insufficient intake can (in a variety of biologically rational ways) often be more stressful than excessive consumption, and – contrary to popular belief – it’s very common for people to underestimate their requirements, and overestimate their intake.

Exposure to chronic stress of various kinds can make a person more susceptible to rising levels of a number of different substances produced in the body which, as part of an overall defensive process, can significantly suppress metabolism.

“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 for survival. Cortisol promotes fat production and storage, often interfering with metabolism and 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 inflammation and metabolic suppression, thereby potentially 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.”

Interference with proper thyroid function due to exposure to polyunsaturated fats occurs at the same time levels of circulating amino acids rise (from cortisol breaking down muscle for fuel). Some of the amino acids are themselves inflammatory and metabolism interfering.

“Obesity is characterized by the activation of the inflammatory process in metabolically active organs in the body…5-HT [serotonin] is an important mediator of inflammatory responses, including obesity…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.”

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

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, estrogen and prolactin and various other inflammatory stress related substances.

“…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”

“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…”

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.

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 is likely to be pro-metabolic in the long run, protecting against polyunsaturated fats, lowering inflammation and helping with the recovery of thyroid and energy systems.

‘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.

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 likely won’t take as much quantity to achieve the results you are after. But not so much because you are eating less calories, rather because you are functioning better and need less and/or burn more.

“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.”

“…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 many safe ways to use diet (or exercise for that matter) to lose weight rapidly. The ways that do work tend to take longer, and do so in a manner which keeps stress low and improves metabolic rate, protecting health as the number one priority.

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

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.

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

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

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

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

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

Circulating progesterone and obesity in men.

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

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


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.

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

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



Image: Original Artist Unknown.

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