Archive for the ‘Obesity and weightloss’ Category

On obesity and diabetes

December 8, 2009

Prompted by this link

Obesity and diabetes (T2DM) are close to my heart; I carry too much weight, was diagnosed with T2DM several years ago, and have struggled to regulate BG. That said, I have successfully kept the important variables within satisfactory limits (just) and avoided recommendation of drug prescription by my GP.
There is no doubt in my mind that primary causality for the diseases of affluence lie rooted in food and with dietary contrasts between past and present. Additionally, I have first hand experience of a strong link between food and mood.
Casting the net a bit wider causality and explanation for proliferation of chronic illness, particularly so called diseases of affluence, lies in the contrast between past and present habitats. So far as I am concerned the dietary influences and inputs of western developed nations falls under the coverall term of habitat.

The trend towards weight gain is readily observable and manifests itself quite prominently in even young teens. Diabetes UK recently issued a release that seven million people are now reckoned to be ‘pre-diabetic’. (“Risk factors include having a close family member with type 2 diabetes, being overweight and having high blood pressure.” Really helpful, that!)

100,000 new cases of T2DM were recorded in 2007; 150,000 in 2008. Off the back of an envelope one would expect 230,000 in 2009. I have the envelope before me; crude maths extrapolates the diagnoses of 7 million cases of T2DM in the period 2009 – 2015.

Genetics may have a part. Genetic evolution is the mechanism behind the evolution of our species. Human genetic evolution is ongoing and it is in response to habitat.

I’m sorry, IMHO one doesn’t get to 32 stone without ingesting more food than is good for you. However, I do not believe it is simply gluttony or lack of willpower that takes a person there. Evolution is a factor because at no time in the human evolutionary past was it ever so easy to ingest so many calories for so little energy expended. Human evolution has simply not prepared us such a surplus in the caloric subsistence economy. The same can be said for domesticated cats and dogs.

I’m so with Ted. I believe enlightenment lies in the development of an ‘inflammation hypothesis’ underpinned by the ‘eicosanoid hypothesis’. Inflammation at cellular level would influence cellular expression because inflammation disrupts which of the chemical messengers can reach the cell. I would anticipate inflammation may influence genetic expression. If you catch a cold or flu you feel ill, but it is the bodies’ defensive inflammatory responses and disruption to eicosanoids (hormone-like chemicals with regulatory function) that makes us feel so rough. (Save for the symptoms of the respiratory tract the other symptoms of flu are not so dissimilar to poor BG regulation in T2DM.) Put simply, the problem is a breakdown in (physiological) regulation, (.. hmmn.)

I’m guided by author Barry Sears on the following. He knows his eicosanoids; important as eicosanoids are he labels some of them as being ‘bad’ or perhaps bad in excess. Eicosanoid imbalance results in inflammation. Sears calls it ‘slow inflammation’. In ‘The Anti-Aging Zone'(p175) Sears tables the conditions associated with eicosanoid imbalances;
Heart disease
Hypertension
Type 2 DM
Inflammatory diseases
Auto-Immune diseases
Cancer
Depression

While obesity is not in the list Sears does believe his zone diet, controlling insulin and balancing eicosanoids, can aid weight management.

What causes eicosanoid imbalance?
The building blocks of eicosanoids are Essential Fatty Acids (EFAs); omega 6 and 3 in the main. Important as they are it seems you can have too much of a good thing. Either too much omega 6 or too little omega 3 can result in omega imbalance that in turn precipitates eicosaniod imbalance. Too much insulin also precipaitates eicosanoid imbalance, and eicosanoid imbalance may lie behind cravings for carbs.

Too much omega 6 can arise from consumption of too much of certain vegetable oils, generally the cheap and stable ones preferred by the food industry. Wild meat can be a source of omega 3 whereas intensively reared cereal supplemented husbanded meat is significantly lower in omega 3.
John’s book ‘The True You Diet’ is excellent with a terrific chapter headed, ‘Oil Crisis’, which catalysed my interest.

The scandal of our time is the dietary preponderance of high GL carbohydrates coupled to increase in consumption of omega 6 PUFAs from vegetable oils; IMHO it’s the origin of metabolic dysfunction.
It’s worse, because Margarines, high in omega 6, can be supplemented with plant derived (cheap) omega 3 (ALA =- alpha-linoleic acid) and marketed with reference to the functionality of the ‘unique blend of omega 6 & 3’. There’s a catch. Humans have a limited capacity to convert ALA to to ‘good’ eicosanoids. The omega 3 (ALA) trumpeted on certain margarines and even ‘healthy’ oils do not compare with omega 3 of mainly marine origin.

The trouble with attributing causality to genes is adoption of the view, ‘I’m fat because of my genes’, or the false hope of a satisfactory and consequence free genetically engineered intervention or therapy. That said, what passes between our lips will determine genetic expression. Inflammation will determine genetic expression (in concurrence with Jamies’ view on Epigenetics). Without doubt aspects of western diet are directing human genetic evolution. What is not known is whether such direction reduces or increases the potential incidence of obesity and/or T2DM for successive generations.

In the field of Paleoanthroplogy there are finger posts to carbs (high GL) and EFA imbalance. Within the mirky waters of epidemiology are pointers to carbs and EFAs. And the functional understanding of EFAs and eicosanoids has pointers to high GL carbs and EFA imbalance.
It can never be too late in life to address EFA imbalance but possibly there are indicators that dysfunction from former EFA and eicosanoid imbalance may linger. Feeding kids toast spread with margarine looks like a bad start to life.

What is it that stands in the way of mainstream appreciation and progress?
Might, the problem be a breakdown in satisfactory regulation?

Artificial Sweeteners – artificial hope?

September 8, 2009

Dr John Briffa raised the issue of artificial sweeteners in his blog of 4th September 2009 headed: The myriad of reasons why artificial sweeteners may not deliver on their weight loss promise”.

Sooner than post at length on Johns blog I posted a reply with link to these paragraphs:-

John, no, I hadn’t researched xylitol any more than having seen it advocated in the aforementioned book. I agree entirely about cause for caution. The entry in Wikipedia reads as though it could have been compiled by those of largely enthusiastic persuasion.
The claim is that spoon for spoon there are 40% fewer calories than sugar but nothing is mentioned about relative sweetness. For all I know one might need to use 40% more of the stuff to satisfy ones palette. There is a link in the wiki to the BMJ; it is not available to me.

What should we regard as natural anyway? Our forebears have a long history of exposure to many sugars intrinsic to many natural food sources including glucose and fructose yet as you point out there is reason to be concerned about fructose and the associated dependency upon the liver to break it down. At 50/50 glucose/fructose common (table) sugar could be labelled natural at one level but considered entirely un-natural by virtue of refinement and context. I guess the same argument holds for the sugar-alcohols (sorbitol, xylitol etc.)
I was not especially advocating xylitol – there seems every reason to categorise it with the ‘artificial sweeteners’; and by the same token, might there be a case to argue that sucrose and perhaps even honey deserve inclusion in that same category?

If human progenitors existed for substantial periods largely as folivores and frugivores we might consider that we ought to be well adapted to these dietary components; fruit and veg in general are deemed to be good for us.
However it could be a pitfall to overlook the contrast between modern cultivars and naturally occurring sources as was. Modern varieties have resulted from the pursuit of sweetness and size. Our ancestors quite likely could not select just the ripest fruits while foraging but probably had to consume unripe or, most certainly under-ripe, fruits too;  fruits with a considerably higher fibre to sugar ratio than our modern equivalents. There’s another contrast too, one might expect our ancestors to have consumed fruits whole.

So 21st century folks in the main have an artificially sweet tooth(?), consume a diet unnaturally high in GL(?), consume too little (non-cereal) fibre(?), and are intolerant to the taste of foods rich in bitter tasting compounds which may be good for them – such as dark leafy greens(?).
Increased exposure to sweeteners, especially the ‘artificial’ ones, in commonplace products cannot be congruent with the likely benefits of re-educating overly ‘sweet-tooths’.

Because I acknowledge the dietary benefits of fibre and the anti-oxidant properties of limonene I do on occasions consume an orange complete with pith and peel. I expect most folks would find that unpalatable and eccentric practice, yet the declaration serves points in para. 3.

The soft drinks industry (US -‘soda’) is clearly factorial in conditioning folks to sweet-tooths and this has come to the attention of at least one US state, as was reported recently in New Scientist, who advocated increased taxation upon sodas, much like the instance of Dr David Walker who tabled a motion for debate and vote at the Glasgow conference  earlier this year (defeated only by a narrow margin) to increase taxation upon chocolate bars and confections on sale in the UK.

Concluding just a little politically I think there is mileage to be gained from considering the role of regulators on both sides of the Atlantic. Is there scope for improvement in the efficacy of regulation and education?

Eating Breakfast

July 8, 2009

On 3 July 2009 Dr John Briffa posted to his blog with the heading ;

Eating breakfast found to be major boon for diabetics, and why this may be important for non-diabetics too

I noticed a comment by Bryce inquiring why this may be so. It set me musing.

Bryce, I hope this may be of help or, if it has weaknesses, that we might be able to develop it.

I see this one as really quite simple and so might any reader sufficiently open-minded to accompany me to an unconventional viewpoint.

All of life as we know it owes it’s existence to a series of major transitions in evolutionary history. Such transitions are hierarchical; that’s to say preceding events give rise to new opportunities and successive  future opportunities. Mammals, and humans, owe their existence to a greater number of transitions than does pond scum or a shark, say.
The body works at a series of levels. It works as a whole, the ‘me’ sat at the keyboard; it works at the level of the division of function performed by our organs; it works at the level of the individual cell, and all of this is subject to a symbiotic relationship with 500 species of bacteria populating our gut who outnumber our cells by a factor of ten.

Our individual cells have a limited capacity to store or buffer energy, yet need to be supplied with energy 24/7.  At a level up from the single cell our physiology has functionality to buffer energy and manage the distribution of energy to the cells; sinking energy as stored as glycogen in the liver and muscles after eating, then releasing it as required to maintain the level of glucose in the blood within quite fine parameters to meet the energy requirements of the bodies cells.

The newborn baby has a high energy requirement to meet the need for growth but has an underdeveloped capacity to buffer energy; consequentially it will not go long between feeds and will wake in the night. In the baby, the need for constant energy is met by a pattern of ingestion characterised by frequent feeds with short intervals between.

Modern humans use a lot of words ending -ism and -isation. Try pausing and reflecting when you encounter one next time. Generally these words describe some some aspect or degree of complexity of modern human life or society, and let’s face it, it has become really very complex. Few of these words can be applied to the animal kingdom.

Looking at the development of the human diet from an anthropological perspective makes for interesting study. Without going too far back in our linage it is possible to encounter progenitors (species of which humans are directly descended) who scampered around the the floor of an arboreal forest, perhaps having characteristics akin to a rain-forest today. Ivan Crowe (1)  postulates movement into the trees themselves may have been a significant transition. It is suggested by Crowe that the change from foraging on the forest floor to inhabiting the trees is a factor that would drive evolutionary changes in size and form, and particularly the changes in degree of limb articulation that distinguish primates from other creatures and is highly notable amongst humans.

It is thought that during the period of evolution described above that the diet largely comprised of fruits and leaves. We might surmise, that in living in a ‘kitchen garden’, these creatures lived a largely sedentary lifestyle. There is are other reasons to think that, and one is that living largely as folivores and frugivores the energy reward available from these plant food is limited and requires time and effort in digestion. We know that these creatures were able to gather adequate food, else they would have become extinct before we emerged, but very likely it took these creatures most of their waking hours to provision and digest their food. Modern gorillas are not suggested as being a close comparison of these progenitors but they do have some dietary and digestive factors that illustrate some pertinent aspects. Modern gorillas exist largely as folivores, pithivores and frugivores and they have a gut morphology consistent with this. Unlike humans, the gut is large and can digest starch in a process requiring fermentation or suchlike. Gorillas just about meet their basic requirements for energy and little else. They have little freedom from the need to eat and digest. They have a sedentary lifestyle forced upon them. Worse still, they are tied to a specific habitat by specific dietary needs. If there is pressure upon the habitat, lack of versatility inhibits the ability of the gorilla to move on to pastures new. If climate change or human encroachment should threaten the habitat of the gorilla, theirs will constitute an evolutionary cul-de-sac.

Our progenitors once had gut morphology different to ours. Their habitat has long since disappeared, but fortunately in the transition new species emerged that would one day produce you and I as offspring.

To express this very simply;  once it took our progenitors all day to provision their food whereas today we do so in moments, with little thought or occupation, and many of us are guilty of doing this only as an inconvenient disruption from all the other tasks we perform. This is some contrast. It arises because humans have a unique ability to capitalise upon energy. Energy from food as foragers, energy from soil as practitioners of agrarianism, and energy from oil as industrialists.  This is only possible because we have time for these human constructs, meaning the -isms and -isations. How did we go from one extreme to the other?

The short answer is our progenitors and ancestors got lucky. They innovated. But be very clear, I do not imply the usual positive connotation(s) associated with the word. I simply mean that distant ancestors adopted change, largely dietary change, that conferred evolutionary advantage. Change was probably out of need in relation to pressure or change applicable to habitat, and drove the evolutionary physiological changes, perhaps accompanying incremental increase in intelligence, that led to the emergence of homo sapiens. Innovation would be slow and incremental in the transition, permitting the necessary evolutionary adjustments along the way. But the tiny incremental improvements contributed to a ratchet effect resulting in increasing calorific reward in return for calorific effort.

Remember, this is the constraining characteristic of our friends the gorillas. They only marginally satisy calorific reward in relation to calorific need. Sizable clicks of the ratchet are cited as the ability to forage for underground storage organs, USOs, in short  (the modern familiar USOs  might include yams, potatoes, carrots and suchlike), the ability to harness fire for cooking, and the ability to make and develop the use of tools.

Eventually we’d become omnivorous, with physiology to match.  Intelligence had developed, as had versatility, and our ancestors were no longer tied to a specific habitat. A few of them set of from the Rift Valley, so the story goes, and the rest as they say, is history. As our ancestors began the migration to populate all corners of the world they were no longer tied to a pattern of ingestion that involved grazing most of the waking day. I have no claims to be able to support this, but I feel there is predictability in being able to say that the move to inclusion of USOs, or at least the general trend of becoming more adept at securing increasing energy density, may be additionally factorial in the development of brain size and/or function. The accepted view is that amino acids and EFAs are factoria and may have been supplied from animal protein and marrow. I subscribe to that too, but USOs are significantly more dense in energy than the foods previously available, today we would say they have a higher glycamic index than say green leaves and unripe fruits. USOs also require adiitional knowledge and skill to find and forage, perhaps involving simple organic tools to dig, and also they often require pre-consumptive processing to make them paletable and or digestible. Some contain toxins that must be negated by leaching and/or heating. But the higher GI, or energy density, makes the trouble worthwhile. If the body is adapting in tandem and is developing increased capacity to sink glycogen in the muscles and liver then it can go longer between feeds and can sleep longer. So USOs introduce an imperative to pass on skills and knowledge and may also have allowed these ancestors to sleep longer, something that, intuitively, I feel may be factorial in developing intelligence. Certainly, the brain is acknowledged as being highly consumptive of energy.

A corelation in different species between capacity for intelligence and the capacity to store glygogen, liver size, and/or sleeping habits might in part constitute support for this theory, but so far as I know humans are the only primates with any real ability to exploit USOs. This then renders comparison difficult.  I haven’t had time to examine such a possibility. The theory is not much more than thinking aloud.

We have moved on in the story where our ancestors have moved into the paleolithic; the gatherer-hunter period. We shall move on swiftly again to the agrarian age commencing around 20,000 years ago. Up to this time, humans have been lucky to enjoy a relationship with food that has satisfied the basic need and more; successive innovations had improved calorific reward for calorific effort, and time has been released from the imperative to provision food. Those of our ancestors that made it this far had capitalised and improved upon the ability to gather calorific reward as foragers.

The move to agrarianism is a huge click on the ratchet. This is a period of domestication of cereal grain. Aspects of division of labour were likely apparent in the foregoing subsistence lifestyle, and are apparent in those peoples and tribes alive today in remote parts who still continue with subsistence practices, but the move to agrarianism also accompanied increased moves to division of labour and specialising occupations. It was the dawn of the moves to the -isations such as larger, more structured, communities we call civilisations. It was not all plain sailing; some civilisations were lost along the way. But benefits of cooperative behaviours and increased division of labour, coupled with farming practice and a move towards the cultivation of grain resulted in increased food security, at least in terms of availability, that permitted industriousness in other ways. One example of such industriousness being construction of the pyramids.

The point in time is significant. The move to greater reliance upon grain constitutes an enormous click on our ratchet of increasing energy density within the provisioning of food and was so significant that the ability to move towards industrialisation can be attributed to it, at least in the fertile and cyclically replenished growing region of the Nile delta, though the true dawn of industralisation as we accept it today was founded upon the ability to harness motive power and chemical morphology from fossil fuel as an energy source. Grain is significantly higher in GI and becomes even higher in GI if it is refined. Introduction to the diet of grain on this scale was not without it’s impact on human health an skelature that is recorded in the fossil record. The other distinguishing feature of a diet high in cereal grain, discounting the inclusion of meat, is that it is less balanced in protein and carbs as say leaves and tree nuts may be. Save for sugar itself, refined grain is just about as energy dense in carbohydrate as it is possible to get. It is significantly lean in the phytonutrients that would have been supplied in several million years of evolutionary precedent from the diverse range of  plant matter incorporated into the diet. It is lean in comparable fibre too.

Fast forward to the present day; we lead fast lives and eat fast food, we give precious little thought or time to provisioning our food, or how we eat eat, we eat sizeable meals punctuated by sizeable intervals between meals, and the meals themselves are comprised of foods of high GI. The effect of this is that the foods to which we are drawn, and the pattern of our behaviour as regards eating habits, pattern of ingestion, if you like, contributes to a diet of high aggregate glycaemic load. The term glycaemic load is generally applied as a measure of much and how fast carbohydrate from a given foodstuff will spike our blood sugar, but I find the term equally fitting to indicate the blood sugar load and, consequentially, the insulinemic load placed upon the body. This really does test the limits of our physiology and largely because while the capacity to sink glycogen confers upon us a degree of freedom from having to constantly eat in order to maintain our blood sugar, the predictability is that we have hiked up the aggregate GL beyond or ability to sink the glucose spike, beyond the bodies capacity to tolerate long term hyperinsulinemia arising from large, infrequent, meals of high GL and the associated large release of glucose from the gut to the blood, and beyond our capacity to store the excessive spike of glucose as glycogen. The body has contingency for this case,  excess blood glucose can be converted to body fat and used later. I think we are overloading that ability too. It is something that our scampering forest floor dweller did not do and if the contrast between him and us does not in some way cast light upon causality for obesity, insulin resistance, and type2 diabetes then I will eat my own do-dos. At some point in the time line I have described, our pace of innovation has outstripped the potential for evolutionary adjustment, and that point constitutes a tipping point.

The fossil record greatly implicates the introduction of cultivated cereal grain as such a tipping point. I am in broad agreement, but I do not argue the case for not eating grain. I think grain can be included as part of a balanced diet but that balance may vary between individuals. Besides,  for all that I believe a diet of high aggregate GL is implicated as a prime factorial in chronic disease, particularly those whose incidence is often associated with being overweight or obese, I have reached a firm opinion that nature rarely exhibits singularity. Instead I think that nature exhibits pluralism, particularly when the nuts and bolts of nature are scrutinised.  In conversation with a GP upon the topic of causality for obesity and diabetes, I put my postulation to him. He replied by saying he felt that causation was probably multifactorial though he did not allude to alternate factors. While he may not have intended it to be so, I felt that his reply carried a degree of dismissiveness towards my postulation.  Events cut the chat short and prevented any further  expansion of our discourse.  I have not had the opportunity to take up with him since.

To return to the pluralism I have come to expect from nature I am going to say that in addition to the prime factorial I have described above I expect there to be other compounding or mitigating factors in relation to diabetes. All of this is an ongoing work; including the expression of the increasing energy density from food.  To date I have some 6 or 7 compounding or potentially mitigating factors on my radar. This may create the impression of it being complicated. No, I do not regard it as complicated; I simply regard it as being plural. I’m in agreement with the doc who said during our telephone conversation that causation was ‘multifactorial’.  Actually, I’m forming the opinion that the common expectancy of a singular expression of causality is actually what renders things complicated. I can make my explanation sound fairly simple, but rarely can I do it briefly, so I aware of the need to wrap things up.  Time does not permit reference to the several likely compounding factors.

If high GL is attributable as primary causation what can we do about it? Simple, reduce the GL.

Obvious choices are:-

Eat less of high GL food and replace with more foods of mid or low GL

Balance every meal with the inclusion of a balanced amount of protein in relation to carbohydrate.

Do not be preoccupied with eating low-fat.

Include fresh foods of high fibre content, excepting the hard cereal fibre and bran.

And finally, Bryce, to answer your question, eat less but at more frequent intervals, because grazing is good whereas skipping meals only to rush the next meal and to consume in large portions , is not so good. It is less of a load upon the bodies systems.

Before folks passed the tipping point, there probably existed the ability to self regulate appetite. Some people exhibit this today. Others however, in increasing numbers have clearly lost that ability. Hyperinsulinemia looks a likely candidate to as to some explanation of the reason why.

I am not opposed to convenience foods per se, but  firmly believe that processed and convenience has a price. Such foods are often conjured from starch, sugar, and fat with small amounts of more distinguished (and less cheap) ingredients, and short of supplying calorific content they have little other nutritional merit.

I eat grain, I love bread. In my condition I ought to eat less. My interpretation of convenience extends to include cereal grain and especially wheat. So I consider those first steps to grain cultivation as moves to convenience food. Grain is convenient because of calorific yield from the land. Grain is convenient as being energy dense permitting humankind to capitalise upon increased calorific reward from high GI food, and grain is convenient because it can be stored; it is so much less perishable that what came before. Refined wheat flour has a long shelf life. According to Taubes (2) mice will eat wheat grain but will stoically refuse to eat white flour. They clearly recognise something that we do not.

Not all grains are equal. Some could be substituted for wheat or rice consumption to good effect. I still like my bread, though.  I have been overweight for a large part of my adult life, and diagnosed diabetic for about 5/6 years. Enlightenment came to me a little late in life. I am losing weight even though I struggle to practice what I preach and I have so far avoided the necessity to medicate my diabetes.

(1) Ivan Crowe, The Quest For Food

(2) Gary Taubes, The Diet Delusion

Many books have contributed to my opinions. Dr John Briffa, The True You Diet and Baryy Sears, The 7 Day Zone diet catalysed a line of thought that took me a long way and continues to do so. Neil Shubin, Your Inner Fish contributed to my confidence in believing in the predictability of nature, Bruce Lipton, The Biology of Belief helped to cement the idea and expectation of pluralism inherent in nature. Other titles that may have some bearing upon this expression of views include Ungar & Teaford, Human Diet; Its’ Origin and Evolution, Lynn Margulis, The Symbiotic Planet, and Patrick Holford, 100% Heath. A presentation by Craig Sams entitled ‘Peak Oil, Peak Soil and Climate Change’  was the single most pragmatic and optimistic argument that I have been party to, ever.

The ideas expressed in this blog are subject to the laws of copywrite and the author reserves his rights in relation to these. Non of the content may be stored in a retrival system, copied or otherwise reproduced with the authors consent.

Hello world! Just a beginning.

June 15, 2009

Ha! After several months passing comments on other peoples blogs the time time has come to begin blogging myself.

My interest is the relationship between food and health and the relationship and causality between food and chronic illness. Of particular interest is the seeming lack of consensus upon the causal factors giving rise to obesity and type 2 diabetes. The outlook for this is one of a United Kingdom perspective because that is where I hail from.  That said, there ought to be considerable commonality between between this and other developed nations.

Here in the United Kingdom our own Food Standards Agency, while being in possession of a much broader remit also has the stated intention of addressing health issues though promoting healthy eating advice for the consumer. High amongst their concerns they declare are heart disease, (CVD and CHD),  obesity and diabetes.  You might think that this may be quite clear cut objective for the FSA and a simple thing to promote, as I once did, but having taken a much greater interest I am in no doubt that this is indeed an issue that is both complicated and challenges some  accepted wisdom. In short, some of what is widely accepted, entrenched and unquestioned, may well be completely invalid.  Some of the policies of the Food Standards Agency are really open to challenge. They may well be plain wrong.

Obesity and diabetes are of particular interest to me because I am overweight and type 2 diabetic. I’d like to address the issue of my excess weight and better manage my diabetes. I have self managed diabetes for some time with varying degrees of success, but since my doctor does not consider my case to require prescribed medication then I guess I can be pleased thus far. It would be helpful for my desire to lose weight if I knew what caused my weight gain. Too much food and not enough exercise may be a simple and valid explanation. Never in the past have I been able to lose weight solely through diet alone. I have done quite well in the past through taking exercise but exercise is demanding of my time. Rather than slogging it out in the gym I’d be happier simply being active as part of my general lifestyle.

Even prior to six months ago I had held  more than a passing interest in the relationship between food and health but then six months ago I was inspired to renew that interest and in much greater detail. I began reading up again in earnest and chanced upon the work of two authors that really set me thinking. My reading list has grown considerably since and at a pace that outstrips my ability to read on. It has been worthwhile, my insight has grown considerably since then and some of my newly acquired knowledge is indeed revelatory.  I am not clever, I rely upon the writings of others far more learned than I, but I was sparked by a couple of things to begin questioning and reasoning for myself. In a moment of inspiration, i had what I describe as original thought but then immediately qualify by saying as original to me. By that I mean that others may have similar views but in that moment I was unaware of them. I would later feel great relief that the idea I had lighted on was apparent in the writings of a few others.

The idea was akin to a hypothesis regarding obesity and diabetes, but lacking formal training and letters after my name i do not like to overplay the word. The power inherent in the idea was in having reasoned it out for myself. Of course I could not have got there without having been prompted by the two authors but I was  mortified that the idea, being some thoughts on the reasons for the growing and alarming trend in obesity, was not promoted by others. It took me some time, but when I tracked down authors who were offering explanations that were in part along the lines of my idea it did come as some relief. Since then I have found a number of publications that resonate with my thinking. These works are contrary to prevailing mainstream opinion and that is what makes them interesting because some of the commonly accepted messages you and I receive everyday from a number of sources may well be faulted.

This blog will largely be centred upon my endeavours to ditinguish for myself, food good sense from food nonsense. Moreover I want to lose weight. I have done so already though I have some scope to lose more. If I can lose weight without resorting to severe calorie restriction, exercising madly, or resorting to a faddy dietplan then in all likelihood so can you.