Calories, Unicorns and Other Myths.
Weight issues tend to be viewed as a case of one and one makes two. But it’s with the ‘and’ where all the magic happens, and when it comes to popular beliefs regarding the subject, it’s the ‘and’ (aka metabolic function), which is often ignored.
Probably the most harmful of all the myths which exist in relation to the subject of ‘obesity’, is that it is the simple result of excessive food consumption, combined with insufficient ‘exercise’.
Based on this theory, it then follows that sustainable weight loss is achieved, via an increase in physical activity, married with a reduction in the number of calories ingested.
Hidden underneath this premise, lies the almost universally accepted belief that weight gain is necessarily a sign of worsening health, and weight loss, a sign of improvement. Unfortunately, it’s not always as black and white as that.
What almost always ends up being ignored in this tale of ‘one and one’ – or calories in, calories out – is the crucial role played by the ‘and’, that is, metabolism.
Many different potentially stressful things, can, under certain circumstances, have an impact upon proper metabolic function, and biological stress is a concept which can arguably be seen to be at the heart of all scenarios which involve suppression of metabolism.
“…impact that the Great Recession had on individuals’ health…The recession indicator itself is associated with a decrease in fruit intake, a shift of the BMI distribution towards obesity, an increase in medicines consumption, and the likelihood of suffering from diabetes and mental health problems.”
One useful way of understanding the harm that can be caused by stress, is by seeing stress as simply anything placing a demand upon an organism. If this demand is not met, with a sufficient amount of energy, a variety of negative consequences can ensue, as a result of attempts to adapt.
This kind of situation, tends to involve the increased release of a number of interrelated stress substances, all of which have the potential to interfere with proper blood sugar regulation and thyroid energy system metabolism, and this can then cause further disruption to energy supply, and consequently more biochemical stress.
When stress is high or ongoing – and thyroid energy systems are suppressed – this commonly leads to a gradual decrease in the amount of calories being used in a day, as well as an increase in fat storage. Not the intended plan.
“…restricting one’s caloric intake increased total daily cortisol…Chronic stress, in addition to promoting weight gain, has been linked with a host of negative health outcomes such as atherosclerosis, coronary heart disease, hypertension, diabetes, cancer, and impaired immune functioning…”
One thing that happens under conditions of stress – when energy systems are suppressed – is that digestion tends to become sluggish and less than optimal, allowing for bacteria to feed and increase in number.
Some foods are far more likely to promote bacterial overgrowth than others – letting bacteria move further up into the small intestine where they don’t belong – and this can be especially problematic when metabolism is sub optimal and digestion is impaired.
Plenty of high quality experimental evidence has demonstrated the relationship between digestive distress and a rise in levels of numerous things (such as bacterial endotoxin) which can promote stress, and damage metabolic function, and many of them have also been shown to be related to weight gain and obesity.
The stress of exercise and calorie restriction, can suppress energy metabolism, and reduce intestinal barrier function, which can allow for endotoxin – and other rising anti-metabolic stress substances like serotonin and estrogen – to pass through into the liver.
If the liver becomes overloaded, this can lead to an increase in circulation of endotoxin, serotonin and estrogen, throughout the main system, promoting a rise in systemic levels of inflammation, and further interference with cellular energy metabolism.
Obesity and chronic inflammation always go together, and a suppressed thyroid metabolism and lowered body temperature, is enough to increase inflammatory cytokines, as well as estrogen, serotonin and numerous other inflammatory things.
Greater circulation of the inflammatory stress substances (including nitric oxide), have been shown to contribute to blood sugar dysregulation and insulin issues, causing a further reduction in thyroid energy system function, and often eventually obesity.
Increased circulation of nitric oxide and bacterial endotoxin, are involved in the progression of diabetes, heart disease and cancer, diseases which are commonly seen together with (and can be promoted by) obesity. Nitric oxide and endotoxin have been shown to be factors directly involved in the development and worsening of obesity.
Estrogen interferes with thyroid energy system function, and excessive levels of estrogen in the system have been proposed as a major factor causing obesity. Fat stores (in particular polyunsaturated fats) are a venue for estrogen production, and the inflammatory effects of estrogen and the PUFAs are closely interrelated, so that a vicious circle like state is often created.
“…inflammatory mediators regulate aromatase expression in the human breast as one mechanism whereby they increase the risk of breast cancer, especially in women who are obese…especially in obese individuals…oestrogen formation and aromatase expression in adipose tissue increase with ageing.”
“…estrogen exposure is known to cause weight gain, primarily through thyroid inhibition and modulation of the hypothalamus…women respond to barely sufficient caloric consumption vastly different from men, with fat depots more readily preserved and developed.”
Obesity (and metabolic issues in general) are known to increase during menopause, and this would likely be far less confusing, if not for the physiologically incorrect and misleading highly popular belief, that menopause is an estrogen deficient state.
But menopause has in fact been demonstrated to be a thyroid function deficient, progesterone deficient, ‘estrogen dominant’ state (with increasing amounts of estrogen trapped inside tissue, not showing up in blood tests), and there is good reason why this kind of biochemical combination, promotes obesity in both women and in men. Treatment with thyroxine (T4), instead of T3 or T4/T3 (especially under circumstances such as this), often makes matters worse.
Excessive stress – which can be the result of too much exercise, or insufficient, inappropriate fuel intake combined with exercise – wastes glycogen stores, stimulating cortisol and adrenaline release. This provokes the liberation of free fatty acids into the bloodstream, interfering with the use of sugar as fuel for the cell, suppressing oxidative metabolism, and further promoting estrogen levels.
Interference with the ability of the cell to effectively use sugar for energy (increasing lactate and lowering carbon dioxide) is central to the promotion of obesity, and there is also evidence, which shows that obesity encourages aerobic glycolysis and cancer progression.
“Obesity is attendant to profound metabolic changes that promote tumor growth…cancer cells, in contrast to normal cells, subsist primarily (although not exclusively) on glucose metabolism via aerobic glycolysis, regardless of oxygen availability.”
Even though a ‘stress metabolism’ can sometimes result in fat loss combined with wasting of muscle and other valuable tissue (commonly promoted as a health improvement), it’s equally likely to cause the kind of metabolic slowdown, that encourages muscle loss, fat storage, and eventually, excessive weight gain.
High cortisol and a shift towards the release of fat into the blood (particularly when polyunsaturated), have been shown to promote estrogen issues, and obesity (as well as related issues like inflammation, chronic hyperglycemia and insulin resistance), yet it’s increasingly common for the blame to be placed on excess calories from sugar.
The problem with immediately blaming sugar and ‘excess calories’ for obesity, is that it is sugar restriction (and calorie restriction in general) which tends to increase stress, and increasing biochemical stress by these methods, exacerbates the metabolic issues which have been closely associated with the promotion of inflammation and obesity.
It might seem illogical to think that more exercise – and less calories – can lead to increased fat deposition, but as stress rises, as blood sugar becomes dysregulated, and thyroid energy system function is suppressed, this becomes more likely.
In any case, if weight loss is achieved through stressful, metabolism damaging means, it is rarely able to be sustained over the long term, nor is it always a sign of improved health, as it generally involves excessive stress, inflammation, and the loss of valuable muscle and other important tissue. In fact rapid weight loss can often be more dangerous than having excess weight, going hand in hand with increased aging, and a susceptibility to many stress related diseases.
Foods which promote stress – and which can be especially obesogenic – include those which are high in the polyunsaturated fats (PUFAs), and some other anti-thyroid ingredients (gums, heavy metals etc.), as well as many kinds of difficult to digest, bacteria promoting fibers and starches.
Nuts, seeds, grains, beans and legumes, and too many under cooked vegetables, are often high on the list. The combination of starchy foods with PUFAs, can have powerful blood sugar interfering effects, helping to push conditions in the direction towards the promotion of fat storage.
It might sound counter-intuitive, however, gradually increasing intake of sugar calories – if the diet includes enough easily digestible protein, vitamins and minerals – can be a good way to reduce stress, and improve metabolism, so as to safely get rid of excess weight over time.
If a person is underweight and wants to gain weight – or if weight gain is an unwanted by-product of stress reduction during the healing process – it is preferable for the added weight to come from excess sugar consumption (being converted into the anti-inflammatory saturated and omega-9 fats), rather than excessive fat consumption (which usually leads to exposure to, and accumulation of, PUFAs).
By providing energy and suppressing stress, sugar can help limit exposure to the stress substances (including endotoxin, serotonin, estrogen, cortisol, nitric oxide, lactate and the polyunsaturated free fatty acids) which cause chronic inflammation, and lead to insulin resistance and obesity, and are central to what makes rapid weight gain (or loss) potentially dangerous.
“…findings support a hypothesis of translocated gut bacteria as a potential trigger of obesity and diabetes, and suggest that the antidiabetic effects of bariatric surgery might be mechanistically linked to, and even the result of, a reduction in plasma levels of LPS [endotoxin].”
“Lactate metabolism is altered in obesity. Increasing obesity is associated with increased blood lactate levels after an overnight fast…We conclude that elevations in basal lactate are associated with the development of insulin resistance.”
“…plasma lactate concentration was lowest in the non-obese group with normal glucose tolerance , highest in the obese subjects with Type 2 diabetes, and intermediate in obese individuals with normal glucose tolerance…”
Providing the means to improve metabolism and digestive function (thereby reducing stress substance release into the main system), seems to be a logical way to protect against the chronic inflammatory issues, which lead to the degenerative disease states which include, and are often exacerbated by, obesity.
Sugar reduces the catabolic hormones and helps spare muscle tissue, and when excess sugar gets converted into fat, it is converted predominantly into saturated fat, which can help shift the balance of fat stored in tissue, away from the inflammatory anti-metabolic, obesogenic PUFAs.
Sugar also helps to increase production of pregnenolone and progesterone (and other anti-inflammatory and highly protective hormones), known to help protect against obesity and related metabolic diseases.
Sugar increases metabolic rate, allowing for significantly more calories to be ‘consumed’ from one day to the next. This is the result of different combinations of the above mentioned anti-stress effects, as well as due to direct liver fueling, providing an important boost to thyroid and energy system metabolism.
Improving metabolic function goes hand in hand with increasing carbon dioxide production, reducing the need for nitric oxide and lactic acid, which interfere with the production of energy in the mitochondria. There is evidence showing that high altitude living can be protective against many stress related conditions, including obesity.
The ability of sugar to suppress stress, and limit the release of the polyunsaturated free fatty acids, can help enable cells to use sugar properly, promoting the production of carbon dioxide, and a gradual safe reduction in excess fat stores.
Much evidence has demonstrated that serotonin is produced in response to stress, as a means to limit energy requirements, and in this way, it makes sense that a high serotonin state interferes with energy expenditure, in part explaining why anti-serotonin substances have been shown to protect against obesity and diabetes.
“…peripheral 5-HT plays an important role in metabolic regulation in peripheral tissues, where it suppresses adaptive thermogenesis in brown adipose tissue. Inhibition of 5-HT synthesis reduced the weight gain and improved the metabolic dysfunction…[also] data indicate that increasing the 5-HT activity in the brain may not be a good strategy for anti-obesity treatment.”
Serotonin and estrogen have a powerful symbiotic relationship, and the thyroid interfering impact of both, are promoted by the inflammatory by-products of greater circulation of PUFAs throughout the system. Anything that lowers stress and encourages thyroid metabolism, can help turn this around in the direction of better metabolic performance.
Excessive weight gain (or weight loss) is a metabolic issue. If you can improve metabolic function and lower stress, you can start to safely gain weight (often via increased muscle mass) or gradually lose excess unwanted fat.
I’m not a doctor or a dietician, and none of this is intended as advice, but I have seen lots of evidence showing that a drug like the ‘anti-histamine’ cyproheptadine (Periactin), has been used to lower stress, and improve metabolism and appetite, and even though it might sound contradictory, there is also good reason to think it provides protection against obesity.
Some other things which have been shown to reduce stress and inflammation, and promote metabolic function, include aspirin, activated charcoal, coconut oil, thyroid hormone, progesterone and pregnenolone, doxycycline, salt and sodium bicarb, vitamin D, vitamin A, vitamin E, methylene blue and red light.
A couple of minutes of bag breathing a day can also help lower stress, and promote improved carbon dioxide production and retention, leading to an increase in metabolic rate and calorie usage.
It can be misleading to talk about excessive calorie intake (and insufficient exercise) in relation to obesity, as how many calories a person can take in without ever gaining excess weight, varies a huge amount depending on metabolism. Too much (or the wrong kind of) exercise, promotes stress and inflammation, and often what is needed is more calories, not less.
Milk is a powerful anti-obesity food for a number of reasons. The importance of a high calcium intake (as well as a high calcium to phosphorus ratio), for protection against inflammation and metabolic dysfunction in general, has been known for a very long time, and continues to be demonstrated by science.
Where calories come from is an extremely significant thing. A diet avoiding PUFAs – and limiting fat and starchy fibrous foods in general – with enough protein from skim milk or low fat cheese, and plenty of sugar from sweet ripe fruits, fruit juice, white sugar and honey, makes sense as an approach to improving metabolism and reducing stress and inflammation, protecting against the weight related issues which can arise.
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Vitamin A decreases pre-receptor amplification of glucocorticoids in obesity: study on the effect of vitamin A on 11beta-hydroxysteroid dehydrogenase type 1 activity in liver and visceral fat of WNIN/Ob obese rats
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