Calories, Unicorns and Other Mythological Wonders.

wondrousYou think because you understand ‘one’ you must also understand ‘two’, because one and one make two. But you must also understand ‘and’. ” – Rumi

It’s inside the ‘and’ where all the magic happens, and unfortunately when it comes to the majority of the popularly held beliefs and assumptions surrounding the entire subject of weight loss – or weight gain – it is the ‘and’ which in the end is purged.

Probably the most harmful of all the persistent and deep-rooted myths which exist in relation to the subject of ‘obesity’, is that it is somehow related to the combination of excessive food consumption and insufficient movement or ‘exercise’.

The logical continuation of this argument – based on the same premise – is then always, that weight loss is the natural result of an increase in physical activity married with the effects of a reduction in the number of calories ingested.

Of course, underneath all of this, lies the almost universally accepted belief that one situation is a sign of worsening health, and the other a sign of improvement. Unfortunately, which one is which isn’t always as clear as many might think.

Sadly however, what almost always ends up getting ignored in this tale of one and one – or as some might say, calories in and calories out – is the crucial and somewhat legendary ‘and’, popularly referred to (at least in general terms) as metabolism.

The reality is that there are a large number of things which can impact upon proper metabolic function. In some ways however, it is possible to interpret them all – one way or another – under the umbrella of the physiological effects of stress of various kinds.

A generally useful approach to understanding the concept of ‘stress’ is to see it as any factor (both external and internal) which has the potential to interfere with thyroid function and overall energy metabolism.

One of the consequences of such interference, is the increase in release of a variety of interrelated stress substances, many of which have the potential to impact upon blood sugar regulation as well as further disrupt and eventually subdue metabolism.

When exposure to stress is continuous – and thyroid and energy systems are suppressed – it is a common response for the body to gradually decrease the amount of calories it can burn in a day, thereby increasing fat storage.

One of the first things that happens under conditions of stress – or when thyroid is interfered with – is that digestion can 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 them move further up into the small intestine where they don’t belong – and this is especially true when digestion is already impaired.

There is a large amount of experimental evidence which clearly demonstrates the relationship between digestive distress and the promotion of numerous factors which damage metabolic function, often eventually leading to excessive weight gain.

Not only does stress – even from exercise commonly combined with calorie restriction – lead to an increase in the secretion of bacterial endotoxin, this suppressed metabolic state tends to reduce intestinal barrier function, thereby allowing for a far greater amount of the toxic substances to pass through to the liver.

Increasing endotoxin release promotes serotonin in the intestines, and when the liver becomes overloaded, these and other toxins make their way into the main system increasing estrogen circulation, raising systemic levels of inflammation and further interfering with cellular energy systems.

All of these factors have been shown – both independently and concurrently – to contribute to blood sugar dysregulation as well as obesity and other related metabolic issues.

Stress and the subsequent wastage of glycogen stores – often also resulting from too much exercise, as well as from insufficient or inappropriate fuel intake, or both – quickly stimulates increased cortisol and adrenalin release, ultimately provoking the liberation of greater amounts of free fatty acids into the bloodstream, interfering with the use of sugar as fuel for the cell.

Although it is possible under some circumstances for this kind of stress metabolism to result in the rapid wasting of muscle and other valuable tissue as well as fat stores – popularly promoted as something to aim for as a means to improving health and well being – it is equally likely to eventuate in the type of metabolic slowdown that causes excessive fat storage and weight gain.

Both rising cortisol as well as the shift towards the release of fat into the blood (particularly when polyunsaturated) are known to promote obesity – and related factors such as inflammation, chronic hyperglycemia and insulin resistance – and yet the blame is increasingly being placed upon excess calories, in particular from sugar.

This is, however, far from being a biologically accurate reflection of the truth, and any attempt to solve issues such as these by restricting the consumption of sugar – or simply calories in general – is likely to only increase stress, thereby exacerbating existing metabolic issues and in many cases eventually leading to further weight gain as well as other related health issues.

Even though it might seem illogical to think it is possible to do more exercise – whilst eating less and less calories – and still end up storing increasing amounts of fat on your body, this is more and more the case as stress rises, interfering with proper blood sugar regulation as well as suppressing thyroid function.

If on the other hand, ongoing – even intermittent – restriction of overall calorie intake ends up resulting in continuous and rapid weight loss, this is rarely something which can reliably be perceived as sustainable over the long term, nor is it likely a sign of an improvement in general metabolic health. The truth is that fast weight loss is sometimes even more dangerous than excessive weight gain, and at the very least often goes hand in hand with an increased rate of aging and susceptibility to degenerative disease.

Foods which promote stress – and can be seen as particularly obesogenic – especially include those which are high in the polyunsaturated fats (and other anti-thyroid chemicals and poisons) as well as the difficult to digest – bacteria promoting – fibers and starches.

Nuts, seeds, grains, beans and legumes, as well as many kinds of often under cooked vegetables are very commonly high on this list. The combination of starchy foods mixed with the polyunsaturated fats have powerful blood sugar dysregulating effects, helping to direct towards conditions which promote fat storage.

It might sound counter intuitive, however, increasing intake of calories from sucrose (and fructose) – in the context of a diet with sufficient protein, vitamins and minerals – can be a safe and effective way to reduce the symptoms of stress and eventually improve metabolic function whilst gradually and safely stabilizing weight.

In cases where a person is underweight – as well as other times where weight is gained as an unwanted by-product of healing metabolism – it is a logical preference for weight increase to be achieved as a result of excess sugar rather than fat (especially the polyunsaturated fats) in the diet.

Sugar helps (both directly and indirectly) to suppress the substances – such as endotoxin, serotonin, estrogen, cortisol and the polyunsaturated free fatty acids – all of which can be a big part of the process leading either to obesity or to rapid and potentially dangerous weight loss. Sugar spares valuable muscle tissue, and when converted into fat helps to shift the balance of fat stored in the tissue to the saturated anti-inflammatory and pro-metabolic fatty acids. On top of all of this, sugar helps to increase production of progesterone (and other protective hormones) shown to help protect against obesity and other related metabolic issues.

Resulting from the combination of all of the above benefits – as well as via the fueling of liver function and the direct boost provided for thyroid and energy metabolism – sugar increases metabolic rate, and allows for significantly more calories to be ‘consumed’ from one day to the next.

The issue of excessive weight gain or weight loss is a metabolic issue. When you improve metabolic function it will eventually allow you to safely either gain the weight – often in part from improvement in muscle mass – you need to gain, or gradually lose the weight you might wish to lose. Although the anti-histamine drug Cyproheptadine (Periactin) is used in many cases to assist in improving appetite for those who suffer from a variety of eating disorders, it presumably does so via stress reduction and the regulation of metabolism. In this sense, it is equally likely to provide protection from obesity, rather than being responsible for causing it.

It’s probably a little misleading – in most cases – to talk about excessive calorie intake (and insufficient exercise) when talking about obesity, as the amount of calories which can be ingested without ever gaining excessive amounts of fat varies significantly according to the state of metabolism. Very often exercise is part of the problem promoting stress, and mostly what is needed is more calories rather than less.

Of course, where those calories come from is significant. A diet (as much as possible) removing the polyunsaturated fats – and significantly limiting starchy fibrous foods as well as fat in general – with enough protein from skim milk and low fat cheese, and plenty of sugar from sweet ripe fruits, fruit juice, white sugar and honey, is one rational approach to dealing with issues relating to weight, arising out of metabolic interference and stress.

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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

Low calorie dieting increases cortisol.

Evidence for metabolic endotoxemia in obese and diabetic Gambian women

Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk.

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

The Association between Visceral Fat and Endotoxin.

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

Circulating progesterone and obesity in men.

Regulation of protein metabolism in middle-aged, premenopausal women: roles of adiposity and estradiol.

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

An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells.

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

Effects of sucrose, caffeine, and cola beverages on obesity, cold resistance, and adipose tissue cellularity.

Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta.


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