Sugar? Fructose? Carbs? What's the Difference!

A friend asked about the difference in impact between blood sugar that is created from excess consumption of carbs that are not sugar, and from carbs that are sugar.  That is to say, why does high carb intake absent a high sugar intake seem to have a different impact than does the high carb/high sugar combination?

First, two facts:
There are islanders who eat at least 60% of their calories as starchy carbs, but they have very little sugar intake.  About 95% of the men smoke.  They have no heart disease.
Additionally, when studied it is often observed that there are healthy fat folks and non-healthy fat folks.

What happens in a very abbreviated answer is that fructose is processed via the liver, and when consumed in excess it seems to make the liver insulin resistant.  This seems to be a stage in development of full insulin resistance.  Insulin resistance is detected as metabolic syndrome, a precursor to diabetes, and a strong predictor of disease in and of itself.

You can find more about various elements of fructose ingestion here:
Fructose link: http://fireofthegodsfitness.blogspot.com/search/label/Fructose

Also, at Gary Taubes blog Gary summarizes three studies on this topic here:
Taubes summary of the three:  http://garytaubes.com/2011/11/catching-up-on-lost-time-–-the-ancestral-health-symposium-food-reward-palatability-insulin-signaling-and-carbohydrates…-part-iib/

The best, most solid science on this topic includes this study:
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057873 ... which is summarized well here:
http://opinionator.blogs.nytimes.com/2013/02/27/its-the-sugar-folks/?_php=true&_type=blogs&_r=0

So here's my concept of the progression:

First, we find those who eat too many carbs, and store them as excess fat, but they are not insulin resistant, do not develop metabolic syndrome, and are healthy by most measures.
Second, we find those who eat "too much" sugar (too much is different by individuals for a variety of reasons like ethnicity, activity level, alcohol consumption, etc) and become insulin resistant.  For these folks, all carbs now become a driver of excess blood sugar, inflammation, and often progress to metabolic syndrome and diabetes.  Once sugar and carbs are reduced, these folks often become normal in their tolerance of non-sugar carbs.
Lastly, we find those with metabolic syndrome and diabetes.  Because they have become insulin resistant, often any kind or dose of carbs will make them fatter and sicker.

The implications for this model include the idea that eating meat, vegetables, nuts and seeds, little fruit or starch and no sugar/wheat is a strong preventative for progression through these stages.  I would bet that it is not possible to eat enough of the above prescription to become insulin resistant.  Once one is in stage 2 or 3 as described above, it may take a more careful approach that includes measured carb restriction, and perhaps induction of ketogenic metabolism.

Notes to a Friend

It's invaluable to have a doc you can trust and yet, doctors have been saying cholesterol and fat intake is the problem in our diet, and that is factually incorrect. The medical profession lost their authority when they abandoned science, which never confirmed that cholesterol CAUSED heart disease.  Cholesterol is a weak predictor of disease, there is almost no benefit to mortality reduction from fat restriction.  The benefits of carb restriction are no longer disputable. I don't know how to help you except to say doctors are as human as any of us, and they no longer have access to more info than you and I do. I know you want to trust your doctor. I would to.

There are two things that may affect the "want a cookie" experience.  One is falling blood sugar - that probably triggers a habitual need for something to stop that from proceeding to blood sugar crash.  That's part of the sugar addiction cycle.  The other part is just an association to pleasure.  The unconscious mind (UCM) always wants to feel pleasure, avoid pain, that is what it does for you.  If cookies distract from pain (and think of the whole cookie eating experience is loaded with guilt, pleasure, surprise, taste, disappointment if its a bad one, etc - these are all great distractions), anytime the UCM can get away from pain by having you eat a cookie.  Obviously that's a short term win, long term loss for "net pain."  

In either case, the way to attenuate the impulse is to have something you can eat that does not derail your blood sugar, but that you like.  This can take a while to find since it's so different for each person.  I use coconut/macadamia nut in a spoon, or coconut and sunflower seeds.  When I'm as lean as I am now, I use coconut on dark chocolate (70% or more).  Sometimes, an egg or avocado will do it (avocado, with salt and champagne vinegar).  Bacon is good too!  Anything that is high in fat and tastes good to you will work.  Over time, this does two things.  One, you don't pit yourself against your hunger or your UCM - that's a losing formula.  Two, you dilute the association between pleasure and cookies.  Three, by not eating cookies it gives your liver time to heal and start processing carbs like it is supposed to

Q: Why would blood sugar be an issue when I'm eating good food?
A:  Hard to know.  Possibly - body expects a sugar bomb every time you eat, prepares by pumping insulin.  That's just a body habit like pavlov's dog, it will stop after eating "right" for long enough

There's a whole part of physiology that goes wrong for folks who eat carbs and especially sugar habitually.  Fat burning enzymes are a use it or lose it prospect, just like everything else in the body.  Your muscles and other tissues run well on fat except for the brain and a few other tissues.  When you don't use fat burning enzymes, the stores of these enzymes decrease.  Then, when you don't eat for a while, you can't convert to fat burning for very long.  The trick to get these stores back up to normal is to deprive your body of exogenous sugar for long enough that the body has to run on fat and rebuild the stores of enzymes in the process.  This can take 1-3 weeks.  It can also feel bad - plus, as you reduce your carb intake, your chronic insulin levels go down, and that allows your tissues to flush excess fluids.  That cycle means you can get low on electrolytes like potassium, sodium and magnesium.  Even moderate dehydration can make a person hungry.  As you eat for health, initially, you have to deliberately drink more water with electrolytes (Smart Water is a good commercial product that does this).  

This is why the "extreme" low carb diets work especially well for reversing metabolic syndrome/diabetes - they keep blood sugar levels so low for so long that the body regains insulin sensitivity, and the liver can get rid of excess liver fat.  This allows the liver to regain insulin sensitivity too.  However, the dehydration/electrolytes issue can be very uncomfortable.  I wouldn't necessarily recommend this for you - your body needs the break from carbs so it can heal, but the heart rhythm issues could be worse in the short term due to electrolyte fluctuations.  You'd need to sip smart water all day long.  Once you get through the 3 week fat burning adaptation period, the appetite regulation, blood sugar regulation, better sleep, rapid weight loss (and all while eating a high fat snack anytime you feel hungry or just feel an impulse to eat) is amazing.  But it's super hard to do by yourself or if you have other demands (work, for example).  Much easier if you are doing this with others.  This is why CF can work so well for lifestyle change - community.

Part of the reason this is important to know is it explains why the idea of no bread no beans no corn tortillas seems so hard - you probably cannot burn fat so you have a true metabolic need for exogenous carbs.  That doesn't always have to be that way, getting fat adapted changes that.

Eat meat, vegetables, nuts/seeds, little fruit/starch, no sugar/wheat, and all the fat you can shove down your pie hole.

Type III Diabetes - ?

To reach her conclusions, de la Monte examined the brains of 45 deceased elderly Alzheimer's patients and found that among those "in the most advanced stage of Alzheimer's, insulin receptors were nearly 80 percent lower than in a normal brain." In healthy brains, insulin stimulates the enzyme that produces the neurotransmitter acetylcholine, the lack of which is seen as a key marker of Alzheimer's disease. In patients with Alzheimer's, de la Monte believes, the brain gradually becomes resistant to insulin.

Previous animal brain studies by de la Monte and others have supported the hypothesis that insulin resistance may be a root cause of Alzheimer's, although many researchers believe that it will emerge as just one of several possible causes, including genetics. Most Alzheimer's patients are not diabetics and while many appear to have insulin-signaling concerns, not all do.

Like Alzheimer's, diabetes has no cure. According to the American Diabetes Association, there are already nearly 26 million diabetics in the country, a number that is growing. Many diabetics do not develop Alzheimer's, but there is measurable overlap and the rates of both diseases are rising. If fatty foods provoke insulin resistance in our brains, then, as New Scientist magazine put it in a recent cover story about the link between diabetes and Alzheimer's, "we may be unwittingly poisoning our brains every time we chow down on burgers and fries."

In the New Scientist article, SUNY-Albany neuroscientist Ewan McNay said: "The epidemic of Type 2 diabetes, if it continues on its current trajectory, is likely to be followed by an epidemic of dementia. That's going to be a huge challenge to the medical and care systems."
http://www.nextavenue.org/blog/alzheimers-really-type-diabetes

This one is a great example of how one wrong conjecture shapes another.

The issue is whether diabetes results from too much ingestion of sugar, or too much ingestion of fat.  For those who have bought the "too much fat is bad" conjecture, the other issues become confusing.  For example, fat in the blood (triglycerides) is a better correlate for heart disease than is cholesterol, and if you reduce carb consumption (especially sugar/fructose) triglycerides decrease significantly for almost all folks.  But fat intake is the problem, right?  But if you eat more fat, lots of fat - up to 85% of total intake - trigs plummet.  Why?  Most likely because when carb intake goes below the toxic level, the liver can stop making trigs out of sugar (especially fructose), and the body learns how to run on fat (in the presence of high sugars, the body will run on sugar).  In short, when the body is fueled with high fat, moderate protein and the right amount of carbs, the body burns fat, does not make much fat in the liver, and regains insulin sensitivity.  These factors are all measurable - so it makes me scratch my head when I read of professionals in the field who still believe that "high fat ingestion" causes diabetes via obesity.

Burgers and fries may play a role in this, but not because they include fat.  It's the bun, the potatoes, ( especially the giant helpings and free refills of Dr. Pepper and other HFCS laden colas) that crush liver function and pile on with excess blood sugar that brings fat burning to a screeching halt and eventually leaves a person with a big belly, insulin resistant, and with chronically high blood sugars (aka, with metabolic syndrome) - almost begging to get alzheimer's or CVD or cancer (which those with metabolic syndrome and diabetes get at disproportionately high rates).

The fact that you can find cultures eating high carb diets (60% carbs), and who smoke heavily (95% in males), and don't have the diseases of civilization, while you can also find populations that eat sugar and don't smoke who do have the diseases of civilization, indicates that sugar (meaning table sugar or HFCS, both of which are 50% fructose) is likely more toxic than are cigarettes.

I think of the rumored last Japanese soldier on some pacific island who was supposedly still waiting as ordered in defense of the turf for the battle with the Americans - who will be the last medical or scientific professional to believe that fat makes you fat and sick, while sugar/carbs are the innocent bystander?

Head Scratcher

It's a head scratcher that an organization like this - the health newsletter of Harvard - is lazily recommending actions that are ten years out of date.  Even the institution's own scientists have moved past the "lowfat to lower cholesterol" fad and back towards science.

The emailed newsletter starts:
"People can reduce cholesterol levels simply by changing what they eat. For example, if you are a fan of cheeseburgers, eating less meat (and leaner cuts) and more vegetables, fruits, and whole grains can lower your total cholesterol by 25% or more. Cutting back on saturated fat (found in meat and dairy products) and trans fat (partially hydrogenated oils) can reduce cholesterol by 5% to 10%."

They recommend these four things to "lower your cholesterol":
"Stick with unsaturated fats and avoid saturated and trans fats.  
"Get more soluble fiber. 
"Include plant sterols and stanols in your diet."

Head scratcher part 1: There's no evidence - after forty years or more of examination - to show that "lower cholesterol" is a benefit for mortality reduction.  Your government, in its infinite wisdom, spent nearly a billion dollars to prove that its advice to reduce cholesterol and fat intake was in fact good for mortality reduction.  Said government failed to show any such thing.  

Second, eating plant sterols and stanols to lower cholesterol is equivalent scratching your private parts to make the sun come up sooner - I guess is might work, but the evidence is sketchy.  Sure, if you believe the conjecture that cholesterol is a cause of early mortality by causing damage to blood vessels, then it might be considered a common sense thing to use a "natural" plant based "food" to lower cholesterol.  But after forty years, and still no direct evidence that cholesterol manipulation via diet (or statin) is helpful for reduced all cause mortality - REALLY?!  A dearly beloved family member would dutifully down benecol every night on a piece of bread and announce proudly that it was "reducing" her cholesterol - how I managed to keep my pie hole shut about that I'll never know.  The kicker?  For females her age, "low cholesterol" correlates with increased mortality.  
The idea that fiber helps mortality is all the rage, but suffers, like the idea of diet to reduce cholesterol, from a lack of evidence.  Why people remain so in love with the idea is a little confusing when there are so many reasons not to down magnum doses of fiber and so little in the way of evidence that fiber is a big benefit - or any benefit.
The topic of cholesterol and causation of disease is very, very complex.  Seems like folks with "high LDL" (which can mean a lot of cholesterol packaged in LDL particles, or a large number of LDL particles, or some combination of both) have a higher correlation with heart disease; but some folks with "normal" LDL die young (Tim Russert being a prime example, his was reportedly 70, which is "low").  HDL has a correlation with reduced mortality, but efforts to raise HDL do not decrease mortality.  Insurance companies - who have a lot more at stake in your health than do your doctors - bet on your ratio of total cholesterol to LDL cholesterol.  
I read this newsletter to gauge changes in the perception of the common view.  At least this perspective - of doing what is best for you based on changes you can verify for yourself without relying upon "expert opinion" - has become obvious for the old guard.  They advise:
"Find the diet that work for you. When a friend or relative tells you how much his or her cholesterol level dropped after trying a particular diet, you may be tempted to try it yourself. If you do and after a few months you discover that you’re not getting the same benefits, you may need to chalk it up to genetic and physiological differences. There is no one-size-fits-all diet for cholesterol control. You may need to try several approaches to find one that works for you.  Although diet can be a simple and powerful way to improve cholesterol levels, it plays a bigger role for some people than for others. If your doctor suggests a lower-fat, lower-cholesterol diet, and despite your best efforts it isn’t working, you may need a different kind of diet, or medication, or both to bring cholesterol down."
It is curious to consider how this will all play out over time.  I don't see a day when all of the "experts" who have advocated low fat and statins to save the world will just have a conference and announce "what we've been telling you was bogus."  At some point, however, the truth will be too obvious for any rational denial.  The "It's the Sugar, Stupid" paper (from Monday and Wednesday's post) will be another nail in the "low fat for health" coffin, making the causality chain something like:
1. Too much sugar causes metabolic derangement (metabolic syndrome)
2. Unchecked, metabolic syndrome progresses to diabetes (full blown loss of glycemic control), and excess carbohydrate in general exacerbates the issue once one is over the metabolic syndrome threshold
3.  Diabetes predicts about a ten year shorter lifespan, and a much shorter period of active life.
The role of fat and cholesterol in this chain is minimal, and if eating high fat and high cholesterol helps you retain glycemic control and avoid metabolic syndrome, we've been in reverso-world the last 30+ years.

It's the Sugar, Folks - NYTimes.com

"Sugar is indeed toxic. It may not be the only problem with the Standard American Diet, but it’s fast becoming clear that it’s the major one."
http://opinionator.blogs.nytimes.com/2013/02/27/its-the-sugar-folks/

Wait - but it's just another epidemiological study, right?  LIke the one AC lambasted on Friday?  Yes, it is, but that does not mean it's wrong!  And, sometimes folks are out to get the one that's paranoid.

This was a unique epidemiological study; not many meet these requirements:

"...and it satisfied the longstanding “Bradford Hill” criteria for what’s called medical inference of causation by linking dose (the more sugar that’s available, the more occurrences of diabetes); duration (if sugar is available longer, the prevalence of diabetes increases); directionality (not only does diabetes increase with more sugar, it decreases with less sugar); and precedence (diabetics don’t start consuming more sugar; people who consume more sugar are more likely to become diabetics).  The key point in the article is this: “Each 150 kilocalories/person/day increase in total calorie availability related to a 0.1 percent rise in diabetes prevalence (not significant), whereas a 150 kilocalories/person/day rise in sugar availability (one 12-ounce can of soft drink) was associated with a 1.1 percent rise in diabetes prevalence.” Thus: for every 12 ounces of sugar-sweetened beverage introduced per person per day into a country’s food system, the rate of diabetes goes up 1 percent. (The study found no significant difference in results between those countries that rely more heavily on high-fructose corn syrup and those that rely primarily on cane sugar.) This is as good (or bad) as it gets, the closest thing to causation and a smoking gun that we will see. (To prove “scientific” causality you’d have to completely control the diets of thousands of people for decades. It’s as technically impossible as “proving” climate change or football-related head injuries or, for that matter, tobacco-caused cancers.)

"But as Lustig says, “This study is proof enough that sugar is toxic. Now it’s time to do something about it.”  The next steps are obvious, logical, clear and up to the Food and Drug Administration."

While I of course disagree with FURTHER government intervention in health and diet (after all, the government is the reason we all chose sugar over fat the last forty years), I'm a big fan of not overdosing yourself on sugar, as regular readers can attest.  Gary Taubes made this case very strongly and this study is if anything a validation of "Good Calories, Bad Calories".
The path through sugar to diabetes and all of the diseases of the west is well trodden and open to all - take the road less travelled by.

Observation: Sugar Is Correlated With Diabetes

Abstract

While experimental and observational studies suggest that sugar intake is associated with the development of type 2 diabetes, independent of its role in obesity, it is unclear whether alterations in sugar intake can account for differences in diabetes prevalence among overall populations. Using econometric models of repeated cross-sectional data on diabetes and nutritional components of food from 175 countries, we found that every 150 kcal/person/day increase in sugar availability (about one can of soda/day) was associated with increased diabetes prevalence by 1.1% (p <0 .001="" after="" and="" biases="" cereals="" controlling="" fibers="" food="" for="" fruits="" including="" meats="" oils="" other="" potential="" selection="" testing="" types="" u="">, total calories, overweight and obesity, period-effects, and several socioeconomic variables such as aging, urbanization and income. No other food types yielded significant individual associations with diabetes prevalence after controlling for obesity and other confounders. The impact of sugar on diabetes was independent of sedentary behavior and alcohol use, and the effect was modified but not confounded by obesity or overweight. Duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes. Differences in sugar availability statistically explain variations in diabetes prevalence rates at a population level that are not explained by physical activity, overweight or obesity.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057873

There's no doubt in my tiny bean that sugar holds a causal relationship with diabetes, and this study would only reinforce such belief.  But the larger point is that this study, and others like it, should never be used to assume causal relationships.

The language tells the tale, even for those who may not be tuned into the philosophy of science.  They tried to account for all the variables, but of course, they don't know all the variables, and there's no guarantee they have accurately weighted the variables they know of.  

For example - how do they possibly know how to control for "fiber" and fiber's so called effects on blood glucose and other issues related to diabetes?  Most of what they think they know about fiber is just a derivative of other observational studies.

Leptin, Low Carb, and Alzheimer's

Abstract 

Accumulation of amyloid-β (Aβ) is a key event mediating the cognitive deficits in Alzheimer's disease (AD) as Aβ promotes synaptic dysfunction and triggers neuronal death. Recent evidence has linked the hormone leptin to AD as leptin levels are markedly attenuated in AD patients. Leptin is also a potential cognitive enhancer as it facilitates the cellular events underlying hippocampal learning and memory. Here we show that leptin prevents the detrimental effects of Aβ_1–42 on hippocampal long-term potentiation. Moreover leptin inhibits Aβ_1–42-driven facilitation of long-term depression and internalization of the 2-amino-3-(5-methyl-3-oxo-1,2- oxazol-4-yl) propanoic acid (AMPA) receptor subunit, GluR1, via activation of PI3-kinase. Leptin also protects cortical neurons from Aβ_1–42-induced cell death by a signal transducer and activator of transcription-3 (STAT-3)-dependent mechanism. Furthermore, leptin inhibits Aβ_1–42-mediated upregulation of endophilin I and phosphorylated tau in vitro, whereas cortical levels of endophilin I and phosphorylated tau are enhanced in leptin-insensitive Zucker fa/fa rats. Thus leptin benefits the functional characteristics and viability of neurons that degenerate in AD. These novel findings establish that the leptin system is an important therapeutic target in neurodegenerative conditions.

http://www.neurobiologyofaging.org/article/S0197-4580(12)00425-3/abstract

I doubt the author's conclusion will lead anywhere.  It is well established that high levels of triglycerides  prevent leptin from crossing the blood brain barrier.  My conjecture - and admittedly this is way over my head but a plausible conjecture none the less - is that this is one of the ways that high carb diets negatively impact development of "AD".
First, high carb diets drive high triglyceride levels, and with subsequent development of insulin resistance, high insulin levels.  The high trigs mean that less leptin will interact in the brain, perhaps creating the effects described above which drive amyloid-B accumulation at faster rates.
High insulin levels means that the body's scavenger system for amyloid-B, insulin degrading enzyme, is busy with insulin and never has time to attend to amyloid-B.
Third, fasting results in the body finding and using as much protein in the body as possible, and there's some evidence that this "protein scavenging" reduces build of of AGEs (a protein damaged by glycation) and other "junk" proteins that wind up in the plaques associated with AD.
Lastly, high blood sugar levels drives higher levels of advanced glycation end products, which are also accelerants in the plaques that characterize AD.

The example of the diabetics is telling - they get AD at higher rates than everyone else.  It would be interesting to know - can AD develop in a person who maintains normal to low blood glucose across their entire lifespan?  Or, the same question stated differently:  has a person ever been diagnosed with AD who maintained optimal blood sugar levels across a lifetime (or most of a lifetime)?

Elevated Visceral Fat: "Nobody Wants That"

The language that follows is the language of observational/epidemiological studies:

"among obese adults, visceral fat was associated with more than a twofold increased risk of developing incident diabetes (odds ratio 2.42, 95% CI 1.59 to 3.68).  In addition, developing either condition was also associated with markers of insulin resistance including elevated fructosamine levels (OR 1.95, 95% CI 1.43 to 2.67) and elevated fasting blood glucose (OR 1.88, 95% CI 1.38 to 2.56).

But there were no associations with general markers of obesity, including body mass index (BMI) or total body fat."

In other words, "these are interesting correlations."

Not that I would disagree with their conclusions:

"Our study may have implications for understanding differences between metabolically healthy and pathologic obesity."

This is interesting because not everyone that's fat is insulin resistant, and those who are develop illness as much higher rates than those who are not.

This is also interesting:

"In participants without diabetes at baseline, a number of factors were significantly and independently associated with incident diabetes in obese adults:

• Elevated visceral fat: OR 2.42, 95% CI 1.59 to 3.68 (P<0 .001=".001" li="li">
• Elevated systolic blood pressure: OR 1.26, 95% CI 1.07 to 1.48 (P=0.006)
• Elevated fructosamine levels: OR 1.95, 95% CI 1.43 to 2.67 (P<0 .001=".001" li="li">
• Elevated fasting blood glucose: OR 1.88, 95% CI 1.38 to 2.56 (P<0 .001=".001" li="li">
• Weight gain from baseline: OR 1.06, 95% CI 1.02 to 1.10 (P=0.002)
• Family history of diabetes: OR 2.32, 95% CI 1.25 to 4.29 (P=0.008)

"There were no associations for BMI, total body fat, or abdominal subcutaneous fat, they reported." 

Many of the same factors correlated with the development of insulin resistant in those not obese when the study began.

http://www.diabetesincontrol.com/index.phpoption=com_content&view=article&id=13578&cacatid=1&Itemid=17

All in all, this fits a well recognized pattern of illness - high fructosamine levels/high fructose intake, visceral fat, high blood pressure, elevated fasting glucose, weight gain, and family history of diabetes.  

Lucky for us, most of these symptoms are treatable through carb restriction - I recommend starting out at 25-50g/day to stop these symptoms, and after weight/fat/symptom normalization, many will be able to eat more carbs but maintain their wellness.  Eat meat, eggs, vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.

Elevated Sugars Linked to Brain Shrinkage

"Numerous studies have shown a link between type 2 diabetes and brain shrinkage and dementia, but we haven't known much about whether people with blood sugar on the high end of normal experience these same effects. " The study involved 249 people age 60 to 64 who had blood sugar in the normal range as defined by the World Health Organization. The participants had brain scans at the start of the study and again an average of four years later.

Those with higher fasting blood sugar levels were more likely to have a loss of brain volume in the areas of the hippocampus and the amygdala, areas that are involved in memory and cognitive skills, than those with lower blood sugar levels. 

Interesting note:

A fasting blood sugar level of 180mg/dl.(10.0 mmol/l) or higher was defined as diabetes and a level of 110mg/dl(6.1 mmol/l) was considered impaired, or prediabetes. 
This part is the language of an epidemiological study:

After controlling for age, high blood pressure, smoking, alcohol use and other factors, the researchers found that blood sugar on the high end of normal accounted for six to 10 percent of the brain shrinkage. 

http://www.diabetesincontrol.com/index.php?option=com_content&view=article&id=13511&catid=1&Itemid=17

These are interesting results, in that they correlate with the widely held view that high blood sugars are injurious to the nervous system.  In fact, for a while it was fashionable to cause Alzheimer's "Type III Diabetes" or "Alzheimer's of the brain."  However, as the authors noted, epidemiological studies only suggest a possible cause, and prove nothing.  Whether or not the effect is as dramatic as showing a loss of brain tissue in four years, there are many reasons to fear high blood sugar's negative impacts on your health, and zero negative side effects of eating for glycemic control.

Mercola On Fructose

What is the link between fructose and blood pressure? Fructose in your diet raises your blood pressure in three key ways:

1. When your liver breaks down fructose, uric acid is produced as a byproduct. Uric acid also drives up your blood pressure by inhibiting nitric oxide in your blood vessels. Nitric oxide helps your blood vessels maintain their elasticity. When you consume large amounts of fructose, increasing uric acid levels drive up your blood pressure. If your uric acid levels are chronically elevated, you have an increased risk for hypertension, kidney disease, metabolic syndrome and diabetes. Large amounts of fructose also place a great strain on your liver, which is responsible for most of the metabolic burden.
2. As metabolic physician and nutrition expert Dr. Ron Rosedale has explained, insulin stores magnesium. If your insulin receptors are blunted and your cells grow resistant to insulin, you can't store magnesium, so it passes out of your body through urination. Magnesium relaxes muscles; so, when your magnesium level is low, your blood vessels will constrict rather than relax, which further raises your blood pressure.
3. Insulin causes your body to retain sodium, which in turn causes fluid retention. Fluid retention results in elevated blood pressure and can ultimately lead to congestive heart failure.

I strongly advise keeping your TOTAL fructose consumption below 25 grams per day, or as low as 15 grams if you have high blood pressure, are overweight, or diabetic.

The fructose in whole fruits is generally healthy, unless you consume large amounts, and/or in the form of fruit juices or dried fruits. Still, if you have any of the health issues just mentioned and you're consuming large amounts of fruit, you would be wise to restrict your fruit intake to under 15 grams of fructose per day as well until your condition has normalized.

http://articles.mercola.com/sites/articles/archive/2012/09/23/broccoli-health-benefits.aspx?e_cid=20120923_SNL_Art_1

As always with Dr. Mercola's posts, you have to take the good with the bad.  This article starts out by hyping the benefits of broccoli consumption, but the citations indicate the research is mostly epidemiological, which means little to me.  Not that I would disagree with four servings of broccoli per week, but I doubt this would offer the mythical benefit for most of us in terms of improving blood pressure.  

However, I like the model he's proposing above with regards to how we are such a sick, diabetic, hypertensive culture.  And with this issue, we don't have to rely on goofy science to know if it helps.  With carb restriction generally and fructose specifically, most of us will see blood pressure normalization.

I found that after carb restriction, potassium supplementation further normalized my BP, and recently met someone who's doctor recommended potassium for that purpose also, which I thought was good news.

The big takeaway - all these symptoms (high blood pressure, dis-lipidemia, visceral fat, gout, insulin resistance/diabetes) are not discrete illnesses, but representative of excess consumption of carbs in general and sugars (which almost always are about 50% fructose) specifically.

Low-carbohydrate Ketogenic Diet in Type 2 Diabetes - "GOOD"

Abstract
OBJECTIVE: Effective diabetic management requires reasonable weight control. Previous studies from our laboratory have shown the beneficial effects of a low-carbohydrate ketogenic diet (LCKD) in patients with type 2 diabetes after its long term administration. Furthermore, it favorably alters the cardiac risk factors even in hyperlipidemic obese subjects. These studies have indicated that, in addition to decreasing body weight and improving glycemia, LCKD can be effective in decreasing antidiabetic medication dosage. Similar to the LCKD, the conventional low-calorie, high nutritional value diet is also used for weight loss. The purpose of this study was to understand the beneficial effects of LCKD compared with the low-calorie diet (LCD) in improving glycemia.

METHODS: Three hundred and sixty-three overweight and obese participants were recruited from the Al-Shaab Clinic for a 24-wk diet intervention trial; 102 of them had type 2 diabetes. The participants were advised to choose LCD or LDKD, depending on their preference. Body weight, body mass index, changes in waist circumference, blood glucose level, changes in hemoglobin and glycosylated hemoglobin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, uric acid, urea and creatinine were determined before and at 4, 8, 12, 16, 20, and 24 wk after the administration of the LCD or LCKD. The initial dose of some antidiabetic medications was decreased to half and some were discontinued at the beginning of the dietary program in the LCKD group. Dietary counseling and further medication adjustment were done on a biweekly basis.

RESULTS: The LCD and LCKD had beneficial effects on all the parameters examined. Interestingly, these changes were more significant in subjects who were on the LCKD as compared with those on the LCD. Changes in the level of creatinine were not statistically significant.

CONCLUSION: This study shows the beneficial effects of a ketogenic diet over the conventional LCD in obese diabetic subjects. The ketogenic diet appears to improve glycemic control. Therefore, diabetic patients on a ketogenic diet should be under strict medical supervision because the LCKD can significantly lower blood glucose levels.

http://www.ncbi.nlm.nih.gov/pubmed/22673594      HT: @dreades

Emphasis above is mine.  The BLUF:  it was an intervention study (the best kind), it had a relatively large number of subjects, it lasted 24 weeks (not long but not too short), and the test variable was carb intake.  To be ketogenic, carb intake must remain below 50g/day, for most folks.

The underlying defect in obesity and illness is glycemic control, and the LCKD did best in restoring same.

Hyperlipid: Insulin and the Rewards of Overfeeding

The link below will take you to the blog of "Peter of Hyperlipid".  His blogline is telling:
"You need to get calories from somewhere, should it be from carbohydrate or fat?"
The reason this is the question is that protein almost never makes up more than 40% of kcal, and you have to work pretty darned hard to get that much of your kcal from protein.  There are two reasons for that.  One - high protein foods are generally even higher fat (at least, they are if they are of good quality), and two, no one sits around gnawing protein.  It's work, it's high in satiety, and frankly people who have that impulse just get busy and do something else instead.  If you have video of yourself depressed and compulsively eating high quality protein, by all means send it to me, I'll reconsider the above summary of what I consider the facts to be. 
In other words, do your best but you won't get fat eating meat, eggs, bacon, or fish.  If you get 600 kcal/day on protein, you'll be in the range of world class powerlifters for protein intake.  
Peter's blog can be hard to read.  He likes sarcasm and he likes to be subtle.  He's not a big fan of mercy as regards those whom he thinks are using substandard science or logic.
This particular article references the brouhaha that took place last year between blogger and researcher Stephen Guyanet, of Whole Health Source, and science writer Gary Taubes, when Gary confronted Stephen at the Ancestral Health Symposium.  That confrontation brought to a head two competing theories of why carbs make people fat, and why carb restriction makes it easier for fat people to get leaner and more healthy; and why it does so faster than simple calorie restriction.
So what's the study he uses to make his point - that fat regulation is regulated by insulin more than by leptin and the notional "adipostat" that is conjected to be dis-regulated by highly palatable foods (salt, sugar and fat laden foods) - ?  In this case, it is a study in which young healthy "blokes" are overfed to the tune of 2000kcal/day.
That's a lot.  That's enough to theoretically force a weight gain of a pound every two days. Most "blokes" supposedly run on 2700kcal/day, so bumping them up to 4700 kcal means they were eating almost as much as Morgan Spurlock was (of Super Size Me fame or infamy).  Turns out, they were eating a bunch of high carb junk to get the extra kcal, just as Morgan did.  Would you be surprised to find that in the case of these subjects, overeating by 2000 kcal/day of mostly processed carbs made them fat and sick, just like it did for Morgan?  Nope, me either.
As Peter puts the next part:
Now, all you have to do is to go and ask any cutting edge, state of the art obesity researcher and you can be told that hyperinsulinaemia is a consequence of obesity, not a cause, and that carbohydrates are the worlds greatest slimming aid because insulin is a satiety hormone and, oh, did I fall asleep there?????? Sorry.
http://high-fat-nutrition.blogspot.com/2012/06/insulin-and-rewards-of-overfeeding.html?m=1
So what stats does Peter use to prove that it's not fat accumulation that causes excess insulin, but instead the excess intake which causes high insulin which commands storage of fat (and of excess blood sugar as fat)?  Here's the summary:
If insulin resistance is the result of increasing fat mass, then insulin levels should increase as the subjects - lean healthy blokes - gain fat.  However, that's not what happens.  The insulin rates fall as the rate of fat gain falls.  That's a weird one too - if kcal is still excess, why does the rate of fat gain stall?
The chaps gained, from Table 3, 1kg of fat mass in the first week and only 0.5kg of fat in the second week... Oh, I guess this must be because the subjects either (a) sneaked off to the gym in the second week or (b) flushed their Snicker Bars down the loo in the second week, without passing them through their gastro intestinal tract first (good idea!) or (c) got bored with Snickers and stopped finding them rewarding. And of course they disconnected their Actiheart monitors at the gym.
Otherwise how you can eat 2000kcal over your energy expenditure, equivalent to nearly 200g of fat gain per day, and gain a kilo of fat in the first week, then continue to eat an excess 2000kcal/d for a second week and only gain half a kilo of fat? Calories in, calories out, you know the rules. Hmmm, in the second week there are 14,000 excess calories-in, 5,000 stored, very interesting.
We all know the obese lie about calories. It seems probable that so too must experimental subjects, in direct proportion to the duration of their over eating! Now we know. Bit of a milestone paper this one.
Uh, well, let's hope you are not allergic to sarcasm.  But as he explains, what this study shows is exactly what the body should do, which is: become increasingly insulin resistant as the massive over-feeding continues, to protect the cells from damage which results when tissues are "over-stuffed".  The result is hyperglycemia, as the ability of insulin to shunt excess sugar into cells is blunted via "cellular self defense" aka insulin resistance.
Depending upon the individual predilections of the overfed, some may have had fat cells that remains insulin sensitive long after others lost all insulin sensitivity (that would be the endomorphs, folks, whereas the ectomorphs would lose insulin sensitivity the fastest, since they are quite obviously not lipophillic).  Once the insulin resistance progresses far enough, the liver will begin to store the fat that cannot be stuffed into other tissues - intra-abdominal obesity will increase.  With enough fructose, non-alcoholic fatty liver disease will manifest itself, which will accelerate the insulin resistance.
In short - Peter's brilliant analysis has taken an otherwise just plain weird experiment and shown how it provides the predicted result if viewed through the lens of the carbohydrate/insulin hypothesis.  
Eat meat, vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.

Questioning Carbohydrate Restriction in Diabetes Management

Sixty-one patients were included in the study of type 2, or adult-onset diabetes. They were randomized into two groups, where they followed either a low-carbohydrate (high fat) diet or a low-fat diet.
In both groups, the participants lost approximately 4 kg on average. In addition, a clear improvement in the glycemic control was seen in the low-carbohydrate group after six months. Their average blood sugar level dropped from 7.5 to 7.0A1c (58.5 to 53.7 mmol/mol). This means that the intensity of the treatment for diabetes could also be reduced, and the amounts of insulin were lowered by 30%.
Despite the increased fat intake with a larger portion of saturated fatty acids, their lipoproteins did not get worse. Quite the contrary -- the HDL, or 'good' cholesterol, content increased on the high fat diet.
No statistically certain improvements, either of the glycemic controls or the lipoproteins, were seen in the low-fat group, despite the weight loss.
Dr. Fredrik Nyström, who was part of the study, said, "You could ask yourself if it really is good to recommend a low-fat diet to patients with diabetes, if despite their weight loss they get neither better lipoproteins nor blood glucose levels."

http://www.diabetesincontrol.com/index.phpoption=com_content&view=article&id=12814&catid=1&Itemid=17

Dr. Mary C. Vernon and Dr. Bernstein have been treating people with low carbohydrates for years, and subsequently removing or drastically reducing the amount of insulin they are required to use.  It is good to see academicians testing that protocol with such success.

Fructose and Your Monkey, Part 1

In this post, Gary Taubes (GT) examines the carbohydrate hypothesis of obesity, and the role fructose plays within that hypothesis.  In short, the carbohydrate hypothesis of obesity is that the primary cause of obesity is overconsumption of carbohydrate and the resulting cascade of rising blood sugar, followed by the body’s defensive secretion of insulin, which signals for cells to take up fat and sugar from the blood, and signals the liver to convert sugar to fat.  Repetition of this cycle causes insulin resistance, loss of glycemic control, and eventually metabolic syndrome leading to diabetes.  This progression of disease increases the risk of all of the diseases of civilization. 
http://garytaubes.com/2011/11/catching-up-on-lost-time-%e2%80%93-the-ancestral-health-symposium-food-reward-palatability-insulin-signaling-and-carbohydrates%e2%80%a6-part-iib/

Here’s GT’s description of the first paper (he covers three in the post linked above):
… describes an experiment in which rhesus monkeys were fed their usual monkey chow diet supplemented by a daily 300-calorie ration of fructose-sweetened water. After a year, every last one of the 29 monkeys had developed “insulin resistance and many features of metabolic syndrome, including central obesity, dyslipidemia and inflammation.” Four of the monkeys progressed to type 2 diabetes.

The monkeys drank all the fructose-sweetened drinks they were given but reduced consumption by a nearly equivalent amount of monkey chow.  This implies one of two things – either monkeys are well versed in caloric values and have a sharp eye for food quantity (and thus do not need to weigh and measure their food) OR monkeys have a god given feedback system which resulted in their consumption of calories based on their needs.  Because their pre-fructose drink intake and post-fructose drink intakes were so similar, it is reasonable to conclude that the negative outcomes that took place after the switch to fructose drinks – insulin resistance, central obesity, dyslipidemia, and inflammation - are a result of said drink.

There’s a great deal of animal research out there, and much of it is hard to apply to the human animal.  Monkeys certainly have a different GI tract and metabolic adaptations compared to humans.  However, it still seems reasonable to assume that since fructose sweetened beverages now account for 20% or more of the US population’s caloric intake, compared to 5% in 1970 (thanks to how cheaply industry delivers HFCS nowadays), part of the diabesity epidemic is excess fructose consumption.

How much is excess?  I think it depends.  In my humble opinion, it should be safe to ingest about 25g of sugar/HFCS per day for a person who is in good health, metabolically speaking.  That would be about 12-13g of fructose.  If you have metabolic derangement and want to get well, that might be too much – but no one knows for sure. 

My advice is to sell your shares of Coca Cola and Pepsi, trade in the soft drinks for sparkling water, and get well.  Once well, I’ll bet you could relish a weekly sugared drink in good conscience and good health.

NOTE:  The people responsible for putting part 2 of this post before part 1 of this post, have been sacked.

Lustig Via Mercola on Fructose

http://articles.mercola.com/sites/articles/archive/2012/05/07/the-sweetener-that-is-more-dangerous-than-alcohol.aspx?e_cid=20120507_DNL_art_1
In general, one would do well to be sceptical about the idea that any one substance causes anything.  However, the data and the models that support the premise that fructose has a unique and potent role in human illness are significant and worth consideration.  Further, fructose restriction is easy and deprives the human of nothing it needs.  From the link above:

The obesity epidemic threatens not only the health and longevity of a clear majority of people, it also adds a tremendous burden to our health care system. The eight primary diseases related to metabolic dysfunction account for a staggering 75 percent of the healthcare costs in the US.

What are these diseases? Diabetes, non-alcoholic fatty liver disease, hypertension, polycystic ovarian syndrome (aka PCOS), dislipidemia, cancer, cardio vascular diseases, and dementia. I think you could easily attribute the autoimmune spectrum to the same causes, though that is conjecture.

I've been looking for these stats for a long time:
The four diseases listed … are conventionally associated with metabolic syndrome. However, as stated by Dr. Lustig, … other diseases fall within this scope as well. He also explains that while obesity is associated with metabolic syndrome and all of these diseases, obesity is not the CAUSE of them; it is simply a marker. Rather, the underlying cause is metabolic dysfunction, and excessive sugar/fructose consumption is a primary driver of that.

According to Dr. Lustig, 20 percent of obese people have perfectly normal metabolic functioning, and the excess weight will not affect their overall lifespan. Ditto for 60 percent of normal-weight people. However, the MAJORITY of obese people—about 80 percent of them—do not have normal metabolic function, and 40 percent of normal-weight people also suffer from metabolic dysfunction, and are therefore prone to these obesity-related diseases.
In other words, some non-obese people have the same metabolic diseases as the obese, and some obese people don't have the metabolic derrangement, and therefore are not sick, just heavy.
This stat is just plain frightening:
The average American consumes 1/3 of a pound of sugar a day. That's five ounces or 150 grams, half of which is fructose, which is 300 percent more than the amount that will trigger biochemical havoc.
But the stat is also a reason for hope, because the implication is that sugar restriction alone may help a significant number of people to stop or reverse their metabolic injury.

As I’ve blogged about several times, and as more and more folks know, fructose is metabolized differently from glucose. The metabolism of fructose by the liver provides several problems, and accelerates all of the cycles that contribute to metabolic syndrome. And as the article reports, it is suspected that fructose short circuits what we understand as the big drivers in appetite control. Fructose does not drive blood glucose levels higher, and therefore does not stimulate insulin. Insulin’s effect on ghrelin is thought to supress hunger. Fructose also contributes to leptin resistance, meaning it biases the metabolic system towards fat accumulation. Because the majority of fructose is metabolized into fat, in a body that is already in metabolic derrangement, often the fructose derived fat contributes to fatty liver, accelerating the metabolic derrangement. Symptoms include abdominal obesity, high triglycerides, low HDL, and often high blood pressure (and other symptoms like gout, more about which will follow).

As Dr. M reports, this process Over time leads to insulin resistance, which is not only an underlying factor of type 2 diabetes and heart disease, but also many cancers.

Thus he recommends two simple but potent tools to reverse the course of a population wide disease:
Severely restricting carbohydrates (sugars, fructose, and grains), and increasing healthy fat consumption.

How pervasive is fructose consumption?
Fructose is the NUMBER ONE source of calories in the US ... even most infant formulas contain the sugar equivalent of one can of Coca-Cola, which helps explain how six-month old babies can be obese.

So the witch’s brew for obesity would require that one eat many carbohydrates per day (via processed foods including breads, cereals, bagels, waffles, pasta, rice, potatoes, etc), combined with sugar, of which ~50% is fructose. The fructose pummels the liver and leptin signaling, while the glucose overloads the body with blood sugars, resulting in the insulin cascade of fat accumulation, inflammation, and eventually, insulin resistance (also accelerated by fructose’s impact on the liver) progressing to metabolic syndrome progressing to diabetes.

Dr. M recommends total fructose consumption of 25g/day or less for the healthy who wish to remain that way. He presents other detailed recommendations for how to think about fruit consumption and fructose, and what you might be able to tolerate if you already suffer from some metabolic injury.

Are you sick of seeing all the adds for gout medication (the guy toting around the jar full of green gunk)? This is why that product is in such demand:
High uric acid, in particular, is a potent marker for fructose toxicity, so if your levels are above 4 mg/dl for men, 3.5 mg/dl for women ... then you would be wise to avoid all forms of fructose until your levels have normalized—just as you would with high insulin levels.

See Dr. M’s article for a detailed list of how much fructose common fruits contain. 

But this isn't all of the bad news for fructose ingestion - other problems include the fact that fructose is a powerful glycating agent and thus produces a disproportionate quantity of advanced glycation end products (AGEs), which are associated with rapid aging in animals and diabetics.  Fructose has also been shown to strongly support the growth of some cancers, either as a powerful fuel in itself, or by accelerating metabolic derrangment, resulting in higher levels of blood sugar, insulin, and insulin like growth factor 1, all of which help cancers thrive (many cancers derive energy from fermentation, which requires large quantities of sugar). 

While paleo man would not have been likely to have access to the incredible variety of fruits that you and I do by virtue of selective hybridization and world wide exchange of what used to be seasonally available fruits, it seems likely to me that fruit played a potent role in the seasonal cycle of human fertility. Thumbnail version (lengthy discussions of this topic available at chriskresser.com): spring and summer fruits helped paleo man fatten up for the winter, while hormonal shifts associated with longer days stimulated higher outputs of reproductive hormones.  That made it common for paleo man to get busy with paleo woman in the late summer, after which paleo progeny would find their way into the world in the spring – when paleo mom would be able to get enough calories, and dietary diversity, to nourish said progeny in style, and without overmuch worry about the cold.

The power of fructose to help humans fatten has been turned on its head by the invention of what we call “corn”, and our ability to use “corn” to make very inexpensive sweeteners. In 1970, fructose was estimated to provide 5% of calories, and is now estimated at 30% of the population’s calories. It seems likely that change was not an improvement for health and wellbeing, and the dollar costs in the provision of health care have been staggering.  Eat meat, vegetables, nuts and seeds, little fruit or starch, no sugar no wheat.  That the government set its sights on fat instead of sugar and carbohydrates as the culprits for the obesity epidemic was a monumental mis-interpretation of the available evidence.  I leave it to you to draw your own conclusions about the consequences.

High Fat For Type I

The diets comprised of:
(i) 45% carbohydrate, 34% fat, 32 grams fibre per day (higher carbohydrate diet).
(ii) 38% carbohydrate, 43% fat, 20 grams fibre per day (higher fat diet).
After 4 months, HbA1c levels were 1.8% higher in those on the higher carbohydrate diet compared to those on the higher fat diet.
This study reveals that a higher fat diet enables better blood sugar control than a higher carbohydrate diet in type I diabetics.
http://healthydietsandscience.blogspot.com/2012/02/type-i-diabetics-have-better-blood.html

I wonder how many people's mind will be changed by the facts.  This isn't a remarkably low carb diet, I look forward to seeing the next level of research in this arena.

Glucose Control? Pick Up Heavy Stuff

The link below will take you to the abstract of an interesting prospective study.  As always with these studies, it would be impossible to assert cause and effect relationships.  At least, it shows that having more muscle mass is not bad for you, and that perhaps sustaining activities which result in creating and sustaining muscular strength are healthful as regards glycemic control.

Conclusions: Across the full range, higher muscle mass (relative to body size) is associated with better insulin sensitivity and lower risk of PDM. Further research is needed to examine the effect of appropriate exercise interventions designed to increase muscle mass on incidence of diabetes.

http://jcem.endojournals.org/content/96/9/2898.abstract

Beware the Wolf in Sheep's Clothing

I eat about 80g/day of carbohydrates.  The average for Americans is between 300 and 400 grams per day.

Interesting label on a "healthy and nutritious" drink. Note the 33 grams per serving of carbs, with 4 servings per bottle, for a whopping 132 grams of carbohydrate in one bottle.  I would love to know how many purchasers drink this all in one sitting.

So, if you find you need to get a bunch of empty calories but convince yourself that you are doing yourself a favor, here's the ideal solution, which has "NO SUGAR ADDED."  It's also "ALL NATURAL FRUIT."

According to this site, a cup of blueberries has ~21g of carbs.  (http://www.carb-counter.net/fruit/1061)  That means you can get 6 cups of blueberries in just one bottle of this stuff!! Such a deal. 

Here's a smaller version of the same product:

Sorry for the sideways angle, but the numbers are:  2 servings, 29g of carbs per serving, which delivers a  nice daily jolt of 58g of carbs to start your day off on the right track.  I just can't figure out why we have this epidemic of diabetes in our country ...
(Minor edits 4 Jan 12, 2141)

Kresser: Chronic Stress = Obesity

When stress becomes chronic and prolonged, the hypothalamus is activated and triggers the adrenal glands to release a hormone called cortisol. Cortisol is normally released in a specific rhythm throughout the day. It should be high in the mornings when you wake up (this is what helps you get out of bed and start your day), and gradually taper off throughout the day (so you feel tired at bedtime and can fall asleep).
Recent research shows that chronic stress can not only increase absolute cortisol levels, but more importantly it disrupts the natural cortisol rhythm. And it’s this broken cortisol rhythm that wreaks so much havoc on your body. Among other effects, it:

• raises your blood sugar
• makes it harder for glucose to get into your cells ¹
• makes you hungry and crave sugar
• reduces your ability to burn fat
• suppresses your HPA-axis, which causes hormonal imbalances
• reduces your DHEA, testosterone, growth hormone and TSH levels ²
• makes your cells less sensitive to insulin
• increases your belly fat and makes your liver fatty
• increases the rate at which you store fat
• raises the level of fatty acids and triglycerides in your blood

Each one of these consequences alone could make you fat and diabetic, but when added together they’re almost a perfect recipe for diabesity.
http://chriskresser.com/10-ways-stress-makes-you-fat-and-diabetic

In other words, you may need to change more than what you eat to obtain and sustain optimal health.  However, some of these things go together.  Smart exercise helps to regulate lipids, as well as cortisol levels, and improves insulin sensitivity - that's all good.  Good quality sleep, in adequate amounts, also helps to improve your ability to adapt to stressful circumstances - not least because it improves your ability to think clearly and identify what you can and cannot control, and have creativity in identifying options going forward.  Identifying an option to work your way around, through or with stressful demands is a huge stress reliever all on its own.

Demands from the life we choose are inevitable - and not bad, per se.  There are many sad rich, bored, unstressed people as there are sad, poor, stressed people (percentage wise).  How we respond to the demands determines how those demands will impact us.  The more abundant your health, the more capacity you have to adapt to any demand.  This is the point of striving for health in my view - not to live forever, not just to have an optimal appearance, but to have options and resources from within yourself that you may bring to bear when life makes the unexpected demand. 

How It Was Done

John Durant (@johndurant) 12/20/11 1:42 AM Long-time diabetic Kim Jong Il successfully assassinated by Western foods