Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2011. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects 35 percent of adults aged 20 and older.Wow-- this is a massive problem. The prevalence of diabetes has been increasing over time, due to more people developing the disorder, improvements in diabetes care leading to longer survival time, and changes in the way diabetes is diagnosed. Here's a graph I put together based on CDC data, showing the trend of diabetes prevalence (percent) from 1980 to 2008 in different age categories (2):
These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.
The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.
Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.
* In other words, it's the best predictor of future diabetes risk.
** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).
I've been inclined to think that obesity is essentially pre-diabetes, and that type 2s get diagnosed when their fat cells become insulin resistant or "top off" somehow.
ReplyDeleteDo you remember Peter@Hyperlipid's tackling that wacky paper (the one with the biblical verse in the abstract) that had the kernel of fat's role in protecting from excess calories? http://high-fat-nutrition.blogspot.com/2010/03/getting-fat-is-good-official.html
Looking at it this (naive?) way, seeing the diabetes epidemic follow on the heels of the obesity epidemic isn't that surprising to me.
Yes, I believe that industrial foods are largely toxic to the body. But it's not just that they are toxic-they're addictive because they tend to really stimulate your brain and taste buds. They're usually salty, sweet, or tangy-or have some other quality that makes a person continue to eat past satiety, or not to feel full at all-to eat for the sake of eating.
ReplyDeleteBeth,
ReplyDeleteTo dig deeper. It is more of an over-eating epidemic.
" I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready."
ReplyDeleteThat's what I call a cliff-hanger!
Looking forward to it.
As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition,
ReplyDeleteStephan hi,
Clearly you agree with the mainstream view that overnutrition causes insulin resistance and not with Gary Taubes, who is convinced that the causality is the other way around.
Since the Taubes view is getting more and more attention these days, can you outline why you believe that it is mistaken?
One of every three U.S. adults has prediabetes, and most of them don't know they have it.
ReplyDeleteInsulin resistance occurs in most cases of type 2 diabetes and prediabetes. So what causes the insulin resistance? In many cases it’s related to overweight, physical inactivity, and genetics. A high-carbohydrate diet may contribute, especially if the carbs are highly refined/concentrated. A few cases are caused by drugs. Some cases are a mystery.
To overcome the body tissue’s resistance to insulin’s effect, the pancreas beta cells pump even more insulin into the bloodstream, a condition called hyper-insulinemia. Whereas a healthy person without diabetes needs about 50 units of insulin a day, an obese non-diabetic needs about twice that to keep blood sugars in check. Eventually, in those who de-velop type 2 diabetes or prediabetes, the pancreas can’t keep up with the demand for more insulin to over-come insulin resistance. The pancreas beta cells get exhausted and start to “burn out.” That’s when blood sugars start to rise and diabetes and prediabetes are easily diagnosed. So, insulin resistance and high insulin production have been going on for years before diagnosis. By the time of diagnosis, 50% of beta cell function is lost.
Yeah, the stats are disturbing for the sheer prevalence, but these seem to be really crude stats compared to what's out there.
ReplyDeleteThis paper by Cowie et al, "Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006" seems to suggest that diabetes and pre-diabetes are at least as rampant as CDC estimates, but that it is only the rate of diagnosis that has been increasing:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628695/pdf/287.pdf
Chris
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ReplyDeleteI'm under the sway of Peter and I think Dr T of Nephropal/EvMed, in that the hypothesis of diabetes is that it occurs when your fat cells get full and can't buffer excess fat anymore. Further, the process where an over-full fat cell spills free fatty acids (FFAs), then those specifically causing peripheral insulin resistance (we know that free palmitic acid triggers IR), would be an important component.
ReplyDeleteTo Stephan's point, what causes someone to eat enough extra calories to overstuffed their fat cells? A fat mass setpoint in the hypothalamus that is "more" than today's fat mass, always leading the body forward.
To the Taubes point though, the mechanism of why the body would attempt to store an extra calorie as fat rather than as muscle or to burn it is interesting.
I seem to be the exception. Slender and active all my life (68) eating the foods I love incl. whole grains (at times baked my own sourdough bread), lots of fruit (my nemesis!) and veggies and a variety of animal products including meat, fish, dark meat chicken, full fat dairy and eggs, etc. - usually prepared by me from scratch. As a person born in Europe I never found typical American food (especially junk food) appealing.
ReplyDeleteI've started keeping my lab reports since March 2001 and see that my FBS has always ranged from around 104 to 120 sometimes 125. Because until recently 126 was the cutoff date for diabetes, my doctor never said anything.
After reading so much about diabetes I decided to check my own BS and was shocked to see my BS go up to 180 to 200 after eating rice or grapes, etc. I am now 'eating to meter' but my BS never goes below 100. Yet there has been no progression in all those years. And I have no complications.
In summary: I have been slender and active all my life - there is NO diabetes in my family - and I never ate the typical SAD diet.
Thanks Stephen for this post. You also nicely sumarized your view on the pathogenesis of diabetes. I've been looking into this lately and there are several camps or schools of thought-which one is right, or can they both be right?
ReplyDelete1) General over consumption of calories leads to overfatness which leadds to insulin resistance and then diabetes.
2) Over consumption of certain carbohydrates (simple) leads to full glycogen stores which eventually leads to insulin resistance (but not in the fat cells) which eventually leads to adipose insulin resistance and then diabetes.
You seem to be in the first category(?) Others like Robb Wolf and Gary Taubes seem to be in the second.
This maybe too much of a generalization and certainly a massive simplification but there are different schools of though out there-can they both be correct?
Does adipose become insulin resistant first or last?
marie,
ReplyDeleteThe Peter/Dr T hypothesis (for lack of a better name, someone please help me put that better) would suggest that you simply don't have the ability to store much fat, and thus actually can easily have insulin resistance and high blood sugars.
Please read,
http://high-fat-nutrition.blogspot.com/2010/03/getting-fat-is-good-official.html
"Thus, we propose that adipogenesis delays, rather than causes, the metabolic syndrome induced by chronic caloric surplus."
If your body lacks the ability to put on fat (adipogenesis), then you have less buffer to prevent metabolic syndrome.
http://evmedsociety.blogspot.com/2010/07/putting-it-all-together.html
From the data that I have gathered, the adipose tissue hits a cut-off point of capacity. Ischemia may be the inciting factor which leads to production of the inflammatory cytokines IL-6 and TNF-alpha. It is a matter of supply and demand for the adipocytes. As they enlarge, with the addition of fatty acids, there comes a point were the vascular supply cannot meet the metabolic demands of the cell - leading to ischemia. And thus the cytokines IL-6 and TNF-alpha are produced along with PAI-1 (plasminogen activity inhbitor) (1) which increases coagulability.
Again, bad things happen when fat cells can no longer accept more fat.
Things like this:
http://high-fat-nutrition.blogspot.com/2009/09/hepatic-insulin-resistance-through.html
one specific method of developing insulin resistance is by increasing fatty acid acyl-CoA moieties within a cell. Acyl-CoA is a single fatty acid molecule joined to a CoA group and represents an "activated" fatty acid, ready to do things metabolically. In both muscle and liver it appears to be these activated lipids, rather than stored triglycerides, which are the metabolic signal, via JNK1 and serine phosphorylation of IRS1, which is used to down regulates the activity of insulin on glucose control.
and
http://high-fat-nutrition.blogspot.com/2009/09/physiological-insulin-resistance-and.html
The trick to staying alive when glycogen depleted is to keep glucose out of any tissue that can cope without it and save almost all of it for brain use.
So the rule is, when the body is flooded with free fatty acids, all fat using tissues should stop using glucose. They should see those free fatty acids and internalise their GLUT4 transporters so they don't waste brain glucose on dumb muscle.
The message to put this change in place is palmitic acid.
PALMITIC ACID CAUSES INSULIN RESISTANCE. YOU WOULD BE DEAD WITHOUT IT. IT'S ADAPTIVE.
But if palmitic acid is spilling out of an over-stuffed fat cell, then that is NOT an adaptive circumstance, that is pathological.
Need bigger/more fat cells!
Secondly, I'm in the camp that thinks that knowing your fasting blood sugar without knowing your fasting insulin is only getting half the picture. A high fasting blood sugar is not necessarily a bad thing, IF 1) you have low fasting insulin (ie your body isn't concerned about it -- assuming your pancreas isn't already toast!), 2) you have a low/normal HbA1c (ie one measure of damage caused by high blood sugar is not indicating a problem), 3) you aren't experiencing energy level or mood swing issues, 4) other measures of damage like a heart scan come back negative.
It's possible for someone who is fat-adapted (ie their metabolism runs easily and well on fat) to have higher blood sugars without the corresponding damage that someone with metabolic syndrome would have. I think.
Steve, A couple REALLY important things have been left out here.
ReplyDelete1. The diagnostic criteria were changed lowering the fasting blood sugar level needed for a diagnosis from 140 to 125. Much of that curve is due to the awareness of this slowly diffusing through the General Practitioner population.
2. Old people have always become diabetic. The population of the very old has skyrocketed over this period.
In fact, that overall prevalence of diabetes in the population as a whole remains almost identical to what it used to be.
And most importantly, "pre-diabetes" is a poor term. It is actually insulin resistance, and for almost all of those who have it, it will NEVER progress to diabetes. For diabetes to occur you need gene damage.
The huge increase in insulin resistance in most likely response to all that intracellular liver fat made after the addition of high fructose corn syrup to our food supply.
This is politics, not science.
Sorry, I omitted the date when the new, lower, diagnostic criteria for diabetes were adopted: 1998.
ReplyDelete@jnktangent, I'm totally with you re the overeating. I've been meaning to do a blog post on the endocannabinoid system, as I recently found a deck (PPT: http://bit.ly/gD4deV) by a senior resident at Case Western that boggled my mind.
ReplyDeleteTurns out that arachidonic acid is/can be a precursor to one or both of the ECS agonists. One of these, anandamide, is apparently somewhat similar to THC, the substance in marijuana responsible for the high (and pot-induced munchies!). There's been a lot of research into pharmaceutical antagonists, but since the ECS also mediates pain, blocking it isn't such a great idea. I've not delved into it deeply, but so far, I've not seen anyone talking about the implications of increasing or reducing dietary omega 6s.
I was actually so giddy about this that I emailed Dr. Bill Lands about it, who replied that this was an ongoing, "active and potentially revolutionary" area of research ... he also noted that fuel allocation was involved in addition to appetite regulation.
So yes, between this and other appetite moderators, I don't disagree that overeating plays a role. That said, I am also increasingly believing that "obesity" really, really is a wicked problem.* As such, finding any one single explanation is likely to be futile (sorry Gary Taubes!). That said, I'll be curious to see Stephan's new thoughts, especially re the lack of connection to industrial food (which I think owns the lion's share of the blame).
* http://en.wikipedia.org/wiki/Wicked_problem
I don't think it's one factor, but many.
ReplyDeleteAnything that causes endocrine disruption can be suspected, such as pesticides, fire retardants, phthalates, BPA, Teflon, or triclosan. Disruptions to the circadian cycle, such as artificial light or screen time at night and shortened/disrupted sleep patterns, also disturb endocrine function and glycemic control. Other drugs cause either disruptions in glucose control or mitochondrial function, such as steriods or SSRIs. Some substances disrupt gut flora or the gut lining, leading to changes in carbohydrate metabolism or systemic inflammation due to leaky gut - such as gluten, NSAIDs, antibiotic use, formula feeding, iron supplements, an overly hygienic environment, etc.
Then there's inflammation from an number of sources - chronic stress from being in a competitive, stratified society lacking a social safety net and traditional family structures, air pollution and other toxic chemicals http://www.sciencedaily.com/releases/2010/12/101202124246.htm, and an inflammatory diet (much discussed on this blog).
Even excessive sitting causes abnormal fat gain and metabolism, and it's hard to find a person whose work, commute, and/or leisure time doesn't involve excessive sitting. Then there are epigenetic changes that you got from your ancestors being exposed to various factors, including stress or famine.
I don't think a high-carbohydrate diet is causative, nor is a diet high in "traditional" fats, unless one is predisposed (as I am, actually) to either respond to fats with reduced insulin action or sensitivity or already have disturbed glucose metabolism, making the body unable to deal with a glycemic surge, which would then lead to glucose toxicity => beta cell death.
Some people could sail through all this disruption and damage without becoming diabetic or insulin resistant, but if you have one or more of hundreds of mutations that can cause disruptions in glucose control, gaining weight and/or being exposed to any or all of the above can push you over the edge into diabetes.
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ReplyDeleteInsulin resistance seems to come down to the ratio of lean muscle mass to ecotopic/visceral fat around the liver. People naturally tend to loose muscle mass as they get older, so glucose is needed more so by the brain than the skeletal muscle but sugars intake remains high and you get problems. The liver's closer to the islets than peripheral adipose so it hoovers up glucose and fructose first when insulin is released but it quickly saturates with glycogen, so it starts making fat instead. Then you get a fatty liver, it can't regulate blood glucose anymore, insulin rises to the point that adipose tissue grabs it and you start getting overweight.
ReplyDeleteFructose seems to be one of the major loads in making the liver fatty but there's not too much evidence to suggest that it's causing inflammation damage per sae. That probably comes from trans-fats and other wierd stuff, like our modern high-gluten dwarf wheat cultivars.
Fasting seems to be a really good way to de-fat the liver, via glycogen depletion and ketone production.
Hi New York,
ReplyDeleteActually, I agree more with Taubes on this than I do with the mainstream. Taubes acknowledges that calorie intake has increased in the US over the last several decades, leading to increased fat mass. I think it would be difficult to question that. But the question for both of us is "why"? He points out that fat mass is biologically regulated, and increased calorie intake is probably a consequence of a change in the regulatory mechanism, not Americans sitting down as a nation and saying "today, I'm going to start eating 250 extra calories per day", or a lack of willpower. Gary and I agree on that.
Where we disagree is what causes a change in the fat mass regulatory system. He believes it's carbs (particularly sugar), I think carbs per se are not the cause.
Hi Chris,
I just looked at the paper. It seems to suggest that the true prevalence of diabetes has been increasing. In the CDC press release I linked to, they also stated that the true prevalence of diabetes has increased, but that the increase was inflated by changing diagnostic criteria.
Hi Thomas,
I think excessive sugar consumption is part of the problem. I do not think starch is inherently fattening, although it can be fattening under certain conditions, which I'll expand on later. I think the idea that starch is inherently fattening is very difficult to defend.
Hi Jenny,
My post addressed both of your points. I noted that the figure is not adjusted for changing diagnostic criteria, and the figure is also broken down by age category.
Thanks for your perspective on "pre-diabetes", you make a good point.
Ed, I think Peter was joking on that post. You may be referring to Unger's theory of lipotoxicity, which is a bit different from what Peter referred to:
ReplyDeletebit.ly/9B3Nsr
@ rmarie -
ReplyDeleteYour story is mine almost to a T. I'm 44.
Does your blood sugar go back down quickly after the high readings, albeit not much lower than 100?
Have you considered that you might have a monogenic form of diabetes (often termed MODY)? You sound like you might have MODY 2. I thought I did, but the genetic test was negative for me on that. I may have something similar that's even more obscure, though.
Good that you've had no complications. I hope for the same for myself.
Suggestions for reversing fatty liver besides laying off the sugar (fructose) and alcohol?
ReplyDeleteThis comment has been removed by the author.
ReplyDeleteThis comment has been removed by the author.
ReplyDeleteStephan,
ReplyDeleteI have a very interesting perspective on diabetes. My father developed Type 1 diabetes as a child in 1930, and was under the care and/or guidance of the Joslin clinic for his whole life.
Very few people who got diabetes in this time period lived long and his having children was definitely mostly unknown territory when he was considering getting married.
Fortunately, he managed to live to 56 until he was overtaken by amputation after wounds in his feet refused to heal. (I understand that the medical technology surrounding this condition has improved greatly, so maybe he would have not needed an amputation at that stage of his life) He was very fit and exercised vigorously most of his life, which I understand to be one of the cornerstones of the Joslin methods. However, when he died, they did an autopsy and he had and overwhelming amount of arteriosclerosis.
So when we grew up, there was very little knowledge of what would happen to children of Type 1 diabetics. I have three siblings, and none of them has any known pre-diabetic conditions. I am probably the worst, in that certain medicines which I have taken are associated with weight gain and general metabolic disorders.
Is there any more knowledge these days about children of Type 1 diabetics?
David L
I am very interested in your ideas on how to lower the setpoint. I have done a series of 6 day elimination diets which were aimed at 'leaky gut' and have a very strict range of allowed foods. Specifically it was a very low lectin diet but is not low carb or necessarily low calorie, although the limited range of foods tended to make non-hunger eating an unattractive option.
ReplyDeleteThe first time I did it my weight dropped by 3kg and settled there even when I went back to a wider range of food. Every time I have done it my weight has dropped and not rebounded, which seems incredible. I only eat the amount I want to, having learned that dieting just makes me miserable, so I can only conclude that somehow my body now wants to be lighter.
Jin, you should read the fatty liver series on Chris Masterjohn's blog,
ReplyDeletehttp://blog.cholesterol-and-health.com/2010/11/sweet-truth-about-liver-and-egg-yolks.html
http://blog.cholesterol-and-health.com/2010/11/does-choline-deficiency-contribute-to.html
http://blog.cholesterol-and-health.com/2010/12/meeting-choline-requirement-eggs-organs.html
One point to note is that having a fatty liver on a high omega-6 diet is much worse than on a low omega-6 diet.
Ned, I really didn't think Peter was joking, overall, regarding the concept that it's the inability to gain additional fat which causes the cascade into full blow metabolic derangement.
Thank you. I've read Chris Masterjohn's series, and I'm feeling a little dense about whether it is wise for someone who is obese to supplement with choline, or betaine, or SAM-e, etc., beyond reasonable diet changes.
ReplyDeleteThis comment has been removed by the author.
ReplyDeleteAs to the question of why calorie intake has increased throughout the last century, here is a thought.
ReplyDeleteTotal fat intake has remained relatively constant over the past hundred years, but the percentage of fat from animal sources has decreased from 80% in 1910 to 60% in 1970 to about 40% today, with the balance from vegetable sources. The intake of the fat soluble vitamins that come almost exclusively from animal fat has therefore decreased by 50% since 1910.
In 1910 it was estimated by a leading nutritional expert that 50% of calories came from fat. The USDA has estimated that the per cent of calories from fat was 43% in 1970 and about 33% today. Since the consumption of total fat has remained relatively constant and protein intake has changed little, it is apparent that there has been a huge increase in consumption of calories, virtually all from carbohydrates, during the last hundred years.
Perhaps the "change in set point" is the result of the body attempting to satisfy the hunger for the fat soluble vitamins that are no longer in the diet.
Everyone here needs to bear in mind that while obesity can be and often is a symptom of impending diabetes, type 2 diabetes does not only occur in obese people.
ReplyDeleteIf you have some of the other symptoms of metabolic syndrome but do not have overweight, don't make the mistake of assuming your problems are "genetic" or "inherited." You may have a greater epigenetic risk of metabolic syndrome, yes, but there's no reason I can think of for a person to just spontaneously come down with conditions that'll lead to them having a heart attack or a stroke. If you've got high triglycerides, high cholesterol with high VLDL, or high blood pressure, assume you're on the way to diabetes even if you're the same weight you were in high school, and eat accordingly.
I know someone who eats a lot of peanut butter and jelly sandwiches and drinks a lot of Mountain Dew (yes, full-sugar), but also rides his mountain bike a lot (he lives in actual mountains) and is as slender as he was in high school. But he also has high blood pressure. I don't think that is an accident and I think he's just as much at risk as someone who weighs 50 pounds extra and doesn't ride the mountain bike. His onset might be delayed, say, ten more years--but he'll have an onset, I bet.
This whole business of focusing on obesity really upsets me. Slender people take personal offense at the existence of fat people and we're treated like vectors for every imaginable nasty disease out there--but slender people can be, and often are, quite unhealthy as well.
I've been both slender and fat. I've been metabolically deranged at both weights. This is what's wrong with equating slenderness with health. Often it *is* associated with good health--but not always.
Jin: I'm no doctor but based on what I've read, if you've got abdominal obesity and it's obviously not all subcutaneous fat (visceral fat winds up being fatty liver sooner or later), I would supplement the choline. It's from the B vitamin group, and I haven't heard anything about overdose hazards. And if you've got fatty liver owing to a choline shortage then you've better off solving that problem than not. Fat in the liver damages the liver cells; while not everybody with early-stage fatty liver has elevated liver enzymes as a result, if you leave it alone long enough and don't clear it, you could suffer permanent damage later.
ReplyDeletePeople who enjoy liver and/or eggs are at an advantage. You can get choline in supplements too, though. I'm not sure how effective that is compared to dietary sources but for someone who's irredeemably picky it's got to be better than nothing.
Another thought on why calorie intake has increased –
ReplyDeleteWe have engineered foods that are palatable even when we are not really hungry. Hunger often has very little to do with why people drink sodas or eat popcorn during movies or eat a desert after dinner. We have come up with very convenient food that you don’t really have to be hungry to eat.
At my daughter’s daycare, in addition to breakfast and lunch, they get 3 snacks during the day. With the exception of maybe fruit and nuts, there is no way they would eat “real food” that often. But give them a cereal bar or some snack crackers, and well sure they will eat it.
On the weekends they sure don’t ask to be fed 5 times before dinner. Occasionally they might ask for a between-meal snack during the day, but they are asking for snack food. If it is 3:00, and I offer to go ahead and make dinner, they say “nah” – they just wanted a snack.
Might-o'chondri-AL, re the ECS, I wasn't bringing that up re diabetes per se, I mentioned it in response to jnktangent's earlier comment about overeating (which I relate to appetite). Either way, I greatly appreciate your info; I'm definitely curious about it.
ReplyDeleteAs an aside, someone I follow on Twitter just posted a link to a paper looking at o3/o6 balance and the ECS: Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions
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ReplyDeleteHi Mighto'chondri-AL,
ReplyDeleteYou suppose you are right that there has been an increase in protein intake over the last century. The data I was working with showed a relatively constant consumption of total fat, fat as per cent of calories and the breakdown between animal and vegetable fat sources. I did not have the breakdown between protein and carb consumption.
While I was careless (fibbing?)in saying that protein intake was constant, if protein and carbohydrate intake increased by the same amount the bulk of the increase would still be carbohydrates.
The most important factor I believe is the huge increase in consumption of vegetable fats and the decrease in consumption of animal fats which resulted in a decrease in intake of fat soluble vitamins.
There have been many studies that show that increased vegetable fat consumption increases risk of diabetes. Israel has the highest consumption of polyunsaturated fats in the world, and consequently has rates of diabetes, heart disease, cancer and that we in the U.S. have yet to achieve as indicated in the following study:
http://www.ncbi.nlm.nih.gov/pubmed?term=Israel%20diabetes%20incidence%20polyunsaturated%20fat
We will match the Israelis in these achievements if the "nutritionists" have continued success in getting people to substitute "heart healthy" polyunsaturated fats for saturated fats.
very interesting
ReplyDelete@Helen - if it goes to 180 or more it will come down slowy 140 or above. I don't remember exactly BECAUSE I don't let it go down naturally anymore if its high...when I suspect I've eaten something that will spike my BS I will usually verify after 30min or so and then immediately do 60-80 jumping jacks and maybe 10 pushups. That tends to lower it 30-40 points quickly. I'll repeat after a while if necessary.
ReplyDeleteI am not prone to hypoglycemia so it's safe for me and works like a charm. I used to go running for half an hour but this is much more convenient and quick.
My normal post-prandial 2 hour baseline is around 115 - 125 without exercise.
@M - I think what you say about the availability of tasty snackfoods is right on and should be considered much more than it is. When people sit around - they just like to munch on something and/or have a soda...has nothing to do with hunger.
To stop this would take a major overhaul of the food/snack industry which won't happen - too much money in it. Education won't work - we already know all this is not good for us. Only a few people like us are willing to forgo the taste temptation.
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ReplyDeleteMight-o'chondri-AL:
ReplyDeleteI have three other suspects for you:
* SSRIs - started getting widely prescribed around 1990.
* High fructose corn syrup - exploded onto the scene in the 1980s, I believe.
* Hydrogenated vegetable oils - have been with us a while, but got loaded into the food supply more in the last 30-odd years, until getting bad press about five years ago.
maybe it is not insulin resistance that is the problem but the cells are actually glucose resistant? it turns out if your deficient in fat soluable vitamines and minerals your cells cannot handle glucose well due to its explosive nature.
ReplyDeleteglucose and fructose are highly reactive to oxygen. so the cells damage themselves if they let it in without the lipid rafts or buffering from fatty acids and minerals for cellular activity.
my doctor has told me I am headed for type 2, but the so called diabetci diet never helped with it.
fats do not suffer the transport problems of glucose and get into cells without insulin. by the way you still burn fat when insulin levels are high if muscles and organs are glucose resistant, because they are not taking in glucose but are burning fats per adipose tissue chemicals telling it to burn only fat.
a good article to read is the obesity epidemic is metabolic syndrome a nutritional deficiency by stephanie seneff. I highly recomment reading her blog it is free just google her name.
genetics determine how and when you get type 2 if yoru unable to gain fat mass in enviroment of severe glucose intolerance you start to suffer problems sooner as there is not enough fat cells to buffer the excess.
that is why lean people get type 2 they still suffer the same nutritional deficinecy and response at the obese, the obese just have more fat to buffer and slow down progression to type 2.
Stephen, doesn't Dr. Kurt Harris see type 2 as originating from a damaged liver (thus inducing hepatic insulin resistance)? How does this square with your 'over nutrition' hypothesis?
ReplyDeleteMy mom is a nurse who treats old people. SO many of these people have diabetes, it's truly amazing. This is a frickin epidemic.
I really think there is a big opportunity for those of us who understand the some of causes of the epidemic (vegetable oils and fructose -- liver annihilaters, industrial foods, and saturated fat/red meat phobia). China and India are also facing diabetes epidemics -- there are a lot of people who need this information.