In 1968 Gerald Reaven and his colleagues at Stanford University published the first studies showing that: “Most people who are insulin resistant are capable of producing large amounts of insulin in order to compensate and force glucose out of the bloodstream and into the cells that need it for nourishment; if insulin-resistant people cannot produce enough insulin to overcome the resistance, they develop type 2 diabetes. The scientific world did not stand up to applaud, possibly because these findings ran contrary to what doctors of the time absolutely ‘knew’ to be true.” Twenty years later Reaven published the first paper showing that insulin-resistant individuals were at great risk of developing what (Reaven) named Syndrome X, a cluster of abnormalities that is a major (albeit 'unknown') cause of heart disease. It was in 1986 at the conclusion of the Banting Memorial Lecture that Reaven said "…at first blush it appears improbable that there is an association between hypertension, hypertriglyceridemia and hyperinsulinemia …" http://www.agale.com.au/Occam.htm
When I first wrote a blog entitled “Insulin Resistance Information and References” many years ago, a search on Yahoo would reveal two sites; mine and a blog written by Hugh O’Donnell. I have lost contact with Hugh unfortunately. But the battle against ignorance and apathy has been won. A search of bing for insulin resistance on October 3 2009, viz http://www.bing.com/ retrieved links 1-10 of 3,430,000 results! A search on Wikipedia reveals an excellent synopsis of the main clinical features of IR http://en.wikipedia.org/wiki/Insulin_resistance
One unfortunate error that is quoted frequently is that obesity and abdominal adiposity in particular are the cause of IR. Unfortunately that is only half the truth. It is quite simply summarised by understanding that IR in an individual with normal weight will lead to a whole litany of diseases. But if the result of IR is obesity, then the obesity itself leads to increased IR. On the other hand, if IR leads to PCO in a fit young woman, she may not necessarily be overweight. See http://www.agale.com.au/PCO.htm But if that fit trim young woman with PCO has the wrong diet she will have a constant battle with her weight and much to her annoyance will probably get a little pot belly; if then she breaks a leg and does not exercise she may rapidly stack on weight! Or consider the case of the fit young man who keeps himself trim with a “disciplined diet” and exercise; if he has inherited the tendency to IR he may experience episodes of “hitting the wall” during exercise; or he may experience “brain fog” mid morning in his office after a “healthy “ breakfast of cereal.
The terms CHAOS and Metabolic Syndrome were introduced in an attempt to make sense out of a diversity of apparently unrelated clinical features. CHAOS = Coronary artery disease+ Hypertension+ Arteriosclerosis+ Obesity Syndrome; but non obese adults get CH & A due to IR! In my reading of the literature it would appear that the best name is “Insulin Resistance Metabolic Syndrome”. This embraces all of the conditions referred to above but also ensures that the physician learns that IR may have an adverse effect on every organ system in the body; from the skin to the brain; from the gut to the heart; from the joints to the muscles; and so on. If you search insulin resistance on Pubmed http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed you will find thousands of references with numerous references being published in recent months, such is the intensity of research. You may ask why is there so much research on IR? One answer lies in understanding the thrust of Storlien’s research. An extract from his paper in 2002 reads:- “In health muscles use either lipid or carbohydrate as fuel. But in diabetes and obesity (ie in IR), skeletal muscle has difficulty in switching between lipid and carbohydrate fuels……….this is an important aspect of insulin resistance of skeletal muscles” Kelley DE, Goodpaster BH, Storlien L 2002 in Annu Rev Nutr 2002;22:325-46
An excellent summary of the phenomenon of IR was given by Ferrannini in 1993. He drew attention to the fact that IR may be beneficial in situations of stress. This aspect of IR has been neglected to date. Clearly we should speak of increased or decreased IR. Ferrannini wrote: "Down regulation of tissue insulin sensitivity…is a physiological adaptation to an environmental challenge...the IR that accompanies stress of any kind (surgery, trauma, inflammation) spares glucose when supply of nutrients are jeopardised...As stress subsides, insulin sensitivity is fully restored The IR of puberty and pregnancy reflects the need for more insulin to sustain accelerated tissue growth without the dangers of hypoglycaemia.....physiological IR in pregnancy and stress is mediated by transient surge of hormones that have marked insulin antagonistic activity. Liver & Renal failure cause toxic states which increase IR. There are several hormones that have marked insulin antagonistic activity. viz catecholamine, glucagon, growth hormone, cortisol, sex steroids (cf warning of IGT on all OCP)....Insulin is a phylogenetically ancient hormone; it is a potent potentially lethal peptide; there are multiple redundant counter mechanisms in order to curb insulin action." Ferrannini E 1993 Foreword in Bailliere’s Clin Endocin & Metab 7,4 From this concept of IR it is clear that IR may be normal or increased. However in all of the literature where the term “insulin resistance” is used the discussion relates to increased IR. Since the introduction of the glitazones in the treatment of diabetes, the term “insulin sensitisers” has entered the literature; these compounds lower IR.
You are probably curious as to how a diagnosis of increased IR is made. Your doctor may suspect it on history alone; the performance of a fasting blood glucose and insulin is a good starting point, but normal values unfortunately do not exclude the diagnosis. The performance of estimates of blood insulin levels remains controversial. However medical science has at last accepted that an elevated fasting insulin level is “a surrogate of IR”. The HOMA Index and Euglycemic Clamp are still considered to be research tools.
Women should realise that all OCPs and HT may cause “impaired glucose tolerance.” This is simply a manifestation of the action of sex steroids referred to by Ferrannini above. Similarly the stress of infection in glandular fever switches on increased IR and explains the tendency to chronic fatigue following glandular fever; it is as if the body forgets to switch off the increased IR as infection subsides http://www.agale.com.au/CFS.htm This does not mean that women should cease HT after the menopause, but it does mean they must make changes to their diet and lifestyle to compensate if they take the pill or hormone therapy.
Cancer patients need to be aware of the fact that cancer has a sweet tooth. Increased IR will occur in cancer; if the individual has foods with a high GI, this actually promotes cancer growth! In 2000 Patrick Quillin wrote:- “During the last 10 years I have worked with more than 500 cancer patients as director of nutrition for Cancer Treatment Centers of America in Tulsa, Okla. It puzzles me why the simple concept ‘sugar feeds cancer’ can be so dramatically overlooked as part of a comprehensive cancer treatment plan……” http://www.newhope.com/nutritionsciencenews/NSN_backs/Apr_00/cancer.cfm
Furthermore “….insulin resistance may significantly increase the risk of death from colon cancer, particularly among women ... research showed that women with characteristics associated with insulin resistance had 10 times the risk of dying from colon cancer than women without these characteristics.” http://www.agale.com.au/cancer.htm
The litany of IR illnesses appears endless:-
· “…….It seems that disturbances in insulin metabolism, especially insulin resistance, play a role in most pathogenic processes that promote the development of AD (Alzheimer disease )...” Am J Alzheimers Dis Other Demen. 2008 Apr-May;23(2):192-9.
· Miscarriages are often attributed to a “blighted ovum”. But maternal IR is overcome in the second half of pregnancy by hormones secreted from the placenta. Recurrent miscarriage in the first half of pregnancy is one of the manifestations of IR in women!
· The list goes on & on! To find more links to IR, search on Pubmed; eg search insulin resistance gout
This syndrome is controlled (but never cured) by the triad of:- "Diet + Exercise + Weight control".
re DIET:- This should be "An Insulin Aware Diet".
The amount of carbohydrates to be allowed will depend on your response.
re EXERCISE:- This should be a graded exercise program until exercising 30 - 60 minutes aerobic exercise daily + 15-20 minutes of Resistance Training (anaerobic exercise) twice weekly
re WEIGHT:- This should be a weight to give a BMI of between 20 & 25,
but must be such that abdominal adiposity is lost. (36 inches - 91cm for men; 30 inches - 76cm for women).
These are three very difficult prescriptions. In the beginning, simply implement the Insulin Aware Diet which is very similar to the CSIRO " Well Being Diet". As I have said above, the amount of carbohydrates to be allowed will depend on your response. So if you don't improve, you will need to gradually lower the amount of carbohydrates in the diet present in grains and root vegetables & eat a lot more greens; but this must be done in collaboration with a health professional who understands this approach & orders periodic blood tests to assess your progress. Your biggest enemy will be your friends who will tell you that the "Locarb Diet" is dangerous. Rubbish! It is dangerous to drive a car if you don't know the rules of the road and even more dangerous to walk across a road if you are blind! So you must fully understand this syndrome & the dietary implications & regularly report to your local Dr or to me for checks in the beginning on your lipids, uric acid, kidney function, liver function & --- get it right! One Diet does not fit all. Ezrin, Eades, Atkins, Bernstein & Cabot all have one thing in common with William Banting of 1869; namely replacing carbs with leafy green salads and vegetables and ensuring an adequate intake of protein. Even the CSIRO Wellbeing diet, maligned by some vegetarian dietitians, increases protein to 30% of daily intake and emphasises the inclusion of low GI carbohydrates, leafy green salads and vegetables. The balance of macronutrients (P,F,CHO) will depend on age, weight, lifestyle, residual pancreatic beta cell function. “Do you bant?” Only three men in history have been immortalized by having their names enter the English language as verbs. The first was an Irishman, Captain Boycott, whose name entered the language in the 1860s. Another was Louis Pasteur and the third was William Banting, a man who came to have a great impact on many peoples' lives. http://en.wikipedia.org/wiki/William_Banting So if you read about William Banting you will realise that the low carb diet is not a fad diet; it is not new; it has been around since the stoneage!
You will find a lot of information about Insulin Resistance on my webpage at :-
http://www.agale.com.au Simply click on the links in blue at the top of that page for starters!!
You will find it helpful to read "The five stages of Change" & Maslow's "Hierarchy of Needs" which you will find on my web page entitled "Changing our Lifestyles" on http://www.agale.com.au/ChangingOurLifeStyles.htm You will find these easily on the alphabetical listing of all my pages.
Further reading. Just as we learn about the living anatomy and histology by studying the dead, similarly we learn about IR in health by studying diabetes. So the best book I recommend is the book by Bernstein. It has an excellent index; begin by finding and reading the pages on insulin resistance. The book is in most local council libraries; I have found Dymock’s in Rundle Mall, Adelaide to be a reliable source; or order online at amazon.com Look for Diabetes Solution by Dr Richard Bernstein; Pub 1997, Revised 2003; Pub. Little, Brown and Company, Boston New York London; ISBN 0-316-09906-6
Allen E Gale, October 5, 2009
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