Factors Contributing to Increased Platelet Reactivity in People With Diabetes,

Factors Contributing to Increased Platelet Reactivity in People With Diabetes

David J. Schneider, MD

People with diabetes, particularly those with type 2 diabetes, exhibit increased platelet reactivity. Hyperglycemia contributes to greater platelet reactivity through direct effects and by promoting glycation of platelet proteins.

Hypertriglyceridemia increases platelet reactivity. Both insulin resistance and insulin deficiency increase platelet reactivity. Insulin antagonizes activation of platelets. Thus, relative or absolute deficiency of insulin would be expected to increase platelet reactivity. Diabetes is associated with oxidative stress and inflammation. Resultant endothelial dysfunction promotes activation of platelets by decreasing production of nitric oxide (NO) that attenuates platelet reactivity. Oxidative stress accentuates this effect by attenuating activity of NO and promoting platelet activation. Inflammation and platelet activation are reciprocally related. Inflammation promotes platelet activation that, in turn, promotes inflammation. Accordingly, improved metabolic control achieved with regimens that improve insulin sensitivity and preserve pancreatic β-cell function is likely to decrease platelet reactivity and enhance effects of antiplatelet agents.

Platelets from subjects with diabetes exhibit increased reactivity (i.e., increased propensity to activate in response to a stimulus) (1). This review highlights factors that contribute to increased platelet reactivity. Type 2 diabetes is more prevalent than type 1 diabetes and is associated with a substantially increased risk of macrovascular complications. Accordingly, this review focuses on platelet reactivity in subjects with type 2 diabetes. Key aspects of type 2 diabetes are insulin resistance, metabolic abnormalities including hyperglycemia, and systemic abnormalities including oxidative stress and inflammation. The influence of each of these abnormalities on platelet function is addressed.

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Metabolic abnormalities and platelet function

Induction of hyperglycemia and hyperinsulinemia in healthy subjects without diabetes increases platelet reactivity (2). Consistent with this observation, improved glycemic control has been associated with decreased platelet reactivity (3). Hyperglycemia can increase platelet reactivity by inducing nonenzymatic glycation of proteins on the surface of the platelet. Such glycation decreases membrane fluidity and increases the propensity of platelets to activate (4). Osmotic effect of glucose is a second mechanism by which hyperglycemia can increase platelet reactivity (5). We found that brief exposure of platelets in vitro to hyperglycemia or a similar concentration of mannitol increased their reactivity. Activation of protein kinase C is a third mechanism by which hyperglycemia can increase platelet reactivity (6). Protein kinase C is an essential mediator of platelet activation.

People with diabetes exhibit increased expression of the surface glycoproteins Ib and IIb/IIIa (7). These glycoproteins mediate platelet adhesion and adherence. Thus, greater expression would be anticipated to increase the functional activity, if not the reactivity, of platelets in subjects with diabetes. Expression of these adhesion proteins correlates with hyperglycemia reflected by A1C. 

Hyperglycemia appears to promote platelet activity by increasing megakaryocyte production of glycoproteins.

Although hyperglycemia is the sine qua non of diabetes, abnormalities of lipid metabolism are uniformly observed. 

People with diabetes typically manifest hypertriglyceridemia. VLDL that is rich in triglycerides increases platelet reactivity (8). This effect appears to be mediated, in part, by apolipoprotein E. Thus, both hyperglycemia and hypertriglyceridemia increase platelet reactivity in subjects with diabetes.
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Insulin resistance, insulin deficiency, and platelet function

Most people who are destined to develop type 2 diabetes exhibit insulin resistance and consequent hyperinsulinemia for 1–2 decades before manifesting diabetes. During this interval, hyperinsulinemia compensates for insulin resistance and fasting hyperglycemia is not evident. Obesity can induce and exacerbate insulin resistance. Apoptosis of pancreatic β-cells leads to a relative and ultimately absolute deficiency of insulin. Progressive insulin deficiency is seen after type 2 diabetes becomes manifest. Both insulin resistance and insulin deficiency can alter platelet reactivity.

Insulin antagonizes the effect of platelet agonists such as collagen, ADP, epinephrine, and platelet-activating factor (9). This antagonism is mediated by activation of an inhibitory G protein by insulin receptor substrate (IRS)-1 (10). Insulin resistance reflects impaired insulin signaling, predominantly mediated by IRS. 

Thus, resistance by the platelet to the effects of insulin (relative insulin deficiency) or absolute deficiency of insulin attenuates insulin-mediated antagonism of platelet activation and thereby increases platelet reactivity.

Obese subjects who are insulin resistant exhibit increased activation of platelets. Platelet activation identified by the measurement of a thromboxane metabolite in urine and the concentration of CD40 ligand in blood was increased in obese compared with lean women. 

Decreased insulin resistance achieved by weight loss or treatment with pioglitazone (without weight loss) reduced the concentrations of these markers (11). 

Another study quantified the concentration of platelet-derived microparticles in blood; microparticles that are released during the activation of platelets were increased in obese subjects (12). Similar to results in the previous study, the concentration of microparticles was decreased after weight reduction (12). Thus, insulin resistance appears to increase the activation of platelets, consistent with increased platelet reactivity.

As mentioned previously, subjects with type 2 diabetes exhibit progressive deficiency of insulin as a consequence of pancreatic β-cell apoptosis. A consequence of pancreatic β-cell apoptosis is absolute deficiency of insulin. Accordingly, the relative deficiency of insulin imparted by insulin resistance is magnified by the superimposition of insulin deficiency. Platelet reactivity that is increased in obese subjects manifesting insulin resistance will be greater when type 2 diabetes is manifest and accompanied by absolute deficiency of insulin.

A recent study suggests that resistance to the effects of insulin is apparent in pathways independent of IRS in addition to those dependent on IRS (13). Consistent with this observation, platelets from subjects with insulin resistance show diminished sensitivity to the actions of NO and prostacyclin (14,15). NO and prostacyclin are produced by the intact endothelium and retard platelet activation by increasing intraplatelet concentrations of cyclic nucleotides, cyclic guanosine monophosphate, and cyclic adenosine monophosphate. Thus, resistance of the platelet to the effects of these agents promotes increased platelet reactivity. Accordingly, insulin resistance attenuates tonic antagonism of platelet activation and thereby increases platelet reactivity.
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Oxidative stress, inflammation, and platelet function

Diabetes is associated with systemic inflammation and oxidative stress that may contribute to increased platelet reactivity. Superoxide has been shown to increase platelet reactivity (16). One mechanism by which superoxide may increase platelet reactivity is by enhancing intraplatelet release of calcium after activation (17). In addition, superoxide limits the biologic activity of NO (18). Attenuating the effect of NO would be anticipated to increase platelet reactivity. Oxidative stress impairs endothelial function and reduces production of NO (19). Impaired endothelial function also decreases the production of prostacyclin (20). Accordingly, oxidative stress that accompanies diabetes promotes greater platelet reactivity through direct effects on platelets and by inducing endothelial dysfunction. Endothelial dysfunction increases platelet reactivity because of decreased production and effect of NO and decreased production of prostacyclin.

Thrombosis that entails platelet activation is intimately intertwined with inflammation. People with diabetes exhibit increased markers of both platelet activation and inflammation (21). In particular, cross-talk between platelets and leukocytes amplifies leukocyte activation both by platelet activation and by platelet reactivity (22). For example, the release of platelet-activating factor by leukocytes primes platelets for activation and increases the extent to which they activate in response to other agonists (23).

An additional mechanism by which inflammation can increase platelet reactivity is by increasing expression of proteins that participate in the activation of platelets. For example, subjects with diabetes exhibit increased expression of Fcγ receptor type IIa (FcγRIIa) and associated increased platelet activation in response to collagen (24). Inflammation appears to increase expression of FcγRIIa, and attenuation of inflammation decreases expression of FcγRIIa (25). Thus, inflammation that accompanies diabetes contributes to increased platelet reactivity that, in turn, contributes to greater inflammation.
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Summary

Diabetes is associated with increased platelet reactivity. Factors that contribute directly to greater platelet reactivity include metabolic abnormalities such as hyperglycemia and hyperlipidemia, both insulin resistance (relative insulin deficiency) and absolute insulin deficiency, as well as associated conditions such as oxidative stress, inflammation, and endothelial dysfunction. Although antiplatelet therapy is necessary to suppress increased platelet reactivity, control of hyperglycemia with regimens that decrease insulin resistance and prevent apoptosis of pancreatic β-cells should decrease platelet reactivity and enhance the efficacy of antiplatelet therapy by addressing root causes of increased reactivity.
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Acknowledgements

No potential conflicts of interest relevant to this article were reported.
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REFERENCES
1. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, Ramírez C, Sabaté

Student From University Of California Discovers Permanent Cure For Type 2 Diabetes!

Student From University Of California Discovers Permanent Cure For Type 2 Diabetes!

Student From University Of California Discovers Permanent Cure For Type 2 Diabetes!

(CNN) – Ashley Haughman, a student at University Of California, was able to completely cure herself from diabetes without ever using a dime of her own money. Ashley is studying nutrition sciences at University Of California, and for a required research project Ashley thought it would be perfect to use university funds to find out how to ‘reverse’ her Type 2 Diabetes. According to Ashley, “the most expensive piece of it all was actually finding what worked. But the actual solution only cost about $5.

“I struggled with Type 2 Diabetes for over 10 years. I tried things like juice cleanses and special diets, but eventually gave up and decided it was in my genes. But I am a 45 year-old single mother with two kids at home and I am also working towards my degree, so it was hard to deal with the low energy that came with Diabetes. When I was assigned this big research project, I saw it as a perfect opportunity to get a deeper look at the root cause of Diabetes and the natural remedies, and that is when my professor realized that the same oil used to treat pain and anxiety may help Diabetes. The best part of it all is I’ve fully cured my Diabetes and I finally have the energy to spend time with my kids.” – Ashley Haughman

Since the study, Ashley shared this miracle oil with her close friend, Alex, who had been struggling with low energy, anxiety and Diabetes. To make matters worse, she had chronic pain from a hip injury in 2012 that made it hard to get through the day. Alex’s experience with the oil is just as impressive as Ashley’s.

“It’s a miracle oil, it relieves pain and anxiety, helps depression, reverses Alzheimers and completely cures Type 2 Diabetes” – Dr. Sanjay Gupta

Alex is fully cured of Type 2 Diabetes, and also uses Ashley’s cure to alleviate her pain and anxiety.

We sat down with Ashley to ask her more about how she discovered this oil could reverse Type 2 Diabetes and whether or not that is all that she used.

CNN: Tell us, how did you know where to start?

Amanda: To be honest, I really didn’t. I was given a budget for the project by the university, and I spent nearly all of it researching everything under the sun. I looked into previous research, case studies, and even successful diabetes recovery stories of others.

CNN: So, how did you find out about it

Amanda: That’s the crazy part! I was at a medical conference in Denver when I heard the world renowned nutritionist Dr. John Claymore talk about CBD (Cannabidoil) and how it can lower stress, boost the metabolism and lower blood sugar. I decided to see if I could find out more about CBD and the effect it has on Diabetics. Surprisingly, even with it’s effects on blood sugar, there was very little research done on CBD and Diabetes. A few weeks after we began the clinical trial using [product_name] and it helped me cure my Type 2 Diabetes for good.

CNN: Was it expensive to get?

Amanda: It’s actually was not very expensive at all, and thankfully so. I didn’t have a huge budget for the project, and that’s why I chose [product_name]. They make a clinical grade CBD Oil which is completely natural, so they don’t spend a lot to manufacture it. They agreed to provide me with a free 1 month sample for my research and I just paid for shipping! So I got [product_name] for under $5 and was ready to start my study.

CNN: That’s impressive! Could you explain how it works?

Amanda: There isn’t much to it, and that is the appeal of it all. Every morning, I take a few drops of [product_name] and usually feel the effects within 30 minutes. I’m finally free from the usual ‘lows’ I deal with having Diabetes and I feel better than I ever have before!


Since helping her friend Alex, Ashley has helped many others become free from Diabetes by using [product_name].

Did you know Diabetes causes these problems?
Low Energy
Stress
Anxiety
Kidney Faliure
Nerve Damage
Eye Damage
Alzheimer’s Disease
Heart Disease
Depression
[product_name] may be able to help!

For our readers, Ashley Haughman has provided the week by week breakdown of her experience and the link to get a free 1 month sample of [product_name]

Results – Ashley fully cured her Type 2 Diabetes in 5 weeks using [product_name]

1. In the morning, take two droplets of [product_name] with a glass of water.

Week One:

One week after taking [product_name] I was surprised at the dramatic results. My energy level was up, and I wasn’t even hungry. A welcomed side effect of [product_name] is its power to curb the appetite.

Best of all, I didn’t even change anything about my daily routine. On Day 7, I was eating my favorite foods again and was feeling better than I had in years! But I still wasn’t convinced, I wanted to wait and see the results in the upcoming weeks.

Week Three:

After 3 weeks, all my doubts and skepticism had absolutely vanished! I still have a ton of energy. Quite often, around mid day, I would tend to run out of steam. But with [product_name] my energy levels didn’t dip, instead they remain steady throughout the day.

Week Five:

On the fifth week, my final results were shocking. I completely reversed my Type 2 Diabetes by simply taking [product_name] daily! I feel blessed to share this with people who are struggling with Diabetes as well.



HELP ASHLEY WIN THE FIGHT AGAINST DIABETES!

*EDITOR’S NOTE: Ashley has successfully cured 112 men and women from Type 2 Diabetes, and it is now legal in all 50 states. Ashley’s next mission is to have CBD Oil classified as a Medical Treatment by the FDA, which would allow millions of Americans to cure their Diabetes forever (And be covered by Medicaid and Insurance).

This requires thousands of successful cases of people curing their Type 1 and Type 2 Diabetes with CBD Oil, so Ashley Haughman has worked with the official suppliers of [product_name] to temporarily provide free 1 month samples for our readers. If you or a loved one has Type 1 or Type 2 Diabetes, get your free bottle today and permanently reverse your Diabetes just like Ashley did!

**Update: LIMITED FREE SAMPLES AVAILABLE – As of Monday, May 21, 2018 , There Still FREE Samples!

Scientists say diabetes is five separate diseases, and treatment could be tailored to each form.

Could there be five types of diabetes rather than just two?

Scientists say diabetes is five separate diseases, and treatment could be tailored to each form.

Diabetes - or uncontrolled blood sugar levels - is normally split into type 1 and type 2.

But researchers in Sweden and Finland think the more complicated picture they have uncovered will usher in an era of personalised medicine for diabetes. 

Experts said the study was a herald of the future of diabetes care but changes to treatment would not be immediate. 

Diabetes affects about one in 11 adults worldwide and increases the risk of heart attack, stroke, blindness, kidney failure and limb amputation.

Type 1 diabetes is a disease of the immune system, which affects around 10% of people with the condition in the UK. It errantly attacks the body's insulin factories (beta-cells) so there is not enough of the hormone to control blood sugar levels. 

Type 2 diabetes is largely seen as a disease of poor lifestyle as body fat can affect the way the insulin works. 

The study, by Lund University Diabetes Centre in Sweden and the Institute for Molecular Medicine Finland, looked at 14,775 patients including a detailed analysis of their blood.

The results, published in The Lancet Diabetes and Endocrinology, showed the patients could be separated into five distinct clusters. 

• Cluster 1 - severe autoimmune diabetes is broadly the same as the classical type 1 - it hit people when they were young, seemingly healthy and an immune disease left them unable to produce insulin
• Cluster 2 - severe insulin-deficient diabetes patients initially looked very similar to those in cluster 1 - they were young, had a healthy weight and struggled to make insulin, but the immune system was not at fault
• Cluster 3 - severe insulin-resistant diabetes patients were generally overweight and making insulin but their body was no longer responding to it
• Cluster 4 - mild obesity-related diabetes was mainly seen in people who were very overweight but metabolically much closer to normal than those in cluster 3
• Cluster 5 - mild age-related diabetes patients developed symptoms when they were significantly older than in other groups and their disease tended to be milder

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Prof Leif Groop, one of the researchers, told the BBC: "This is extremely important, we're taking a real step towards precision medicine.

"In the ideal scenario, this is applied at diagnosis and we target treatment better."

The three severe forms could be treated more aggressively than the two milder ones, he said.

Cluster 2 patients would currently be classified as type 2 as they do not have an autoimmune disease. 

However, the study suggests their disease is probably caused by a defect in their beta-cells rather than being too fat.

And perhaps their treatment should more closely mirror patients who are currently classed as type 1.

Cluster 2 had a higher risk of blindness while cluster 3 had the greatest risk of kidney disease, so some clusters may benefit from enhanced screening. 

Better classification

Dr Victoria Salem, a consultant and clinical scientist at Imperial College London, said most specialists knew that type 1 and type 2 was "not a terribly accurate classification system".

She told the BBC: "This is definitely the future of how we think about diabetes as a disease."

But she cautioned the study would not change practice today.

The study was only on Scandinavians and the risk of diabetes varies considerably around the world, such as the increased risk in South Asians.

Dr Salem said: "There is still a massively unknown quantity - it may well be that worldwide there are 500 subgroups depending on genetic and local environment effects.

"Their analysis has five clusters, but that may grow."

Sudhesh Kumar, a professor of medicine at Warwick Medical School, said: "Clearly this is only the first step. 

"We also need to know if treating these groups differently would produce better outcomes."

Dr Emily Burns, from Diabetes UK, said understanding the diseases could help "personalise treatments and potentially reduce the risk of diabetes-related complications in the future".

She added: "This research takes a promising step toward breaking down type 2 diabetes in more detail, but we still need to know more about these subtypes before we can understand what this means for people living with the condition."

THE TRUTH ABOUT FAT AND SUGAR IS FINALLY EXPLAINED

With the health credentials of sat-fat up for debate again, we cut to the bone

By Men's Health Posted on April 27, 2017

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Why did it take us so long to realise sugar, not fat, was the enemy? In a move that would make most big pharma companies proud, new research published in JAMA Internal Medicine found sugar companies paid to downplay the white stuff's role in heart disease during the 1960s. Scary stuff, even more so because it's had lasting effects on public perceptions. It's time everyone woke up to the truth about fat and sugar. MH investigates...

This morning, as I do most days, I breakfasted on a three egg omelette cooked in coconut oil, with a whole milk coffee. I enjoyed a wedge of full fat cheese with my lunch, poured a liberal dose of olive oil on my evening salad and snacked on nuts throughout the day. In short, I ingested a fair amount of fat and, as a cardiologist who has treated thousands of people with heart disease, this may seem a particularly peculiar way to behave. Fat, after all, furs up our arteries and piles on the pounds – or at least that’s what prevailing medical and dietary advice has had us believe. As a result, most of us have spent years eschewing full fat foods for their ‘low fat’ equivalents, in the hope it will leave us fitter and healthier.

Yet I’m now convinced we have instead been doing untold damage: far from being the best thing for health or weight loss, a low fat diet is the opposite. In fact, I would go so far as to say the change in dietary advice in 1977 to restrict the amount of fat we were eating helped to fuel the obesity epidemic unfolding today. It’s a bold statement, but one I believe is upheld by an array of recent research.

(Related: The healthy way to add cheese to your diet) 

These days I make a point of telling my patients – many of whom are coping with debilitating heart problems – to avoid anything bearing the label ‘low fat’. Better instead, I tell them, to embrace full fat dairy and other saturated fats within the context of a healthy eating plan. It’s an instruction that is sometimes greeted with open-mouthed astonishment, along with my request to steer clear of anything that promises to reduce cholesterol – another of those edicts we are told can promote optimum heart and artery health.

As we will see, the reality is far more nuanced: in some cases lowering cholesterol levels can actually increase cardiovascular death and mortality, while in healthy people over sixty a higher cholesterol is associated with a lower risk of mortality. Why, exactly, we will come to later.

First though, let me make it clear that until very recently, I too assumed that keeping fat to a minimum was the key to keeping healthy and trim. In fact, to say my diet revolved around carbohydrates is probably an understatement: sugared cereal, toast and orange juice for breakfast, a panini for lunch and pasta for dinner was not an uncommon daily menu. Good solid fuel, or so I thought, especially as I am a keen sportsman and runner. Still, I had a wedge of fat round my stomach which no amount of football and running seemed to shift.

That, though, wasn’t the reason I started to explore changing what I ate. That process started in 2012, when I read a paper called ‘The toxic truth about Sugar’ by Robert Lustig in the science journal Nature.  In it, Lustig, a Professor of Paediatrics who also works at the University of California’s Centre for Obesity Assessment, said that the dangers to human health caused by added sugar were such that products packed with it should carry the same warnings as alcohol. It was an eye-opener: as a doctor I already knew too much of anything is bad for you, but here was someone telling us that something most of us ate unthinkingly every day was, slowly, killing us.

The more I looked into it, the more it became abundantly clear to me that it was sugar, not fat, which was causing so many of our problems – which is why, along with a group of fellow medical specialists I launched the lobbying group Action on Sugar last year with the aim of persuading the food industry to reduce added sugar in processed foods. 

Then earlier this year I had another light-bulb moment. In February Karen Thomson, the granddaughter of pioneering heart transplant surgeon Christian Barnard, and Timothy Noakes, a highly-respected Professor of Exercise and Sports Medicine at the University of Cape Town, invited me to speak at the world’s first ‘low carb’ summit in South Africa. I was intrigued, particularly as the conference hosts are both fascinating characters. A former model, Thomson has courageously battled a number of addictions including alcohol and cocaine, but lately it is another powder – one she labels ‘pure, white and deadly’ – that has resulted in her opening the world’s first carbohydrate and sugar addiction rehab clinic in Cape Town. 

Noakes, meanwhile, has recently performed a remarkable U-turn on the very dietary advice he himself expounded for most of his illustrious career: that is, that athletes need to load up on carbohydrates to enhance performance. A marathon runner, he was considered the poster boy for high carbohydrate diets for athletes – then he developed Type 2 diabetes. Effectively tearing pages out of his own textbook, Noakes has now said athletes – and this goes for those of us who like to jog around the park too – can get their energy from ketones, not glucose. That is, from fat not sugar.

Alongside them were fifteen international speakers ranging from doctors, academics and health campaigners who between them produced an eloquent and evidence-based demolition of “low fat” thinking – as well as suggesting that it is carbohydrate consumption, not fatty foods, which is fuelling our obesity epidemic.

 (Related: Men's Health investigates Britain's diabetes epidemic)

Opening the conference was Gary Taubes, a former Harvard physicist who wrote The Diet Delusion, in which he argued that it is refined carbohydrates that are responsible for heart disease, diabetes, obesity, cancer, and many other of our Western maladies. The book caused controversy when it was released seven years ago, but his message is finally gaining traction. And that message is this: obesity is not about how many calories we eat, but what we eat. Refined carbohydrates fuel the over production of insulin, which in turn promotes fat storage. In other words: it’s not calories from fat themselves that are the problem.

It’s a robust message that was reinforced time and again at the conference. Take Swedish family physician Dr Andreas Eenfeldt, who runs the country’s most popular health blog Diet Doctor. In his home country, studies show that up to twenty three percent of the population are embracing a high fat, low carbohydrate diet. A ticking time bomb you might think – but contrary to expectations, while obesity rates are soaring everywhere else, they are now starting to show a decline there. 

More research on this correlation is yet to be done – but in the meantime The Swedish Council on Health Technology has made its position clear. After a two year review involving sixteen scientists, it concluded that a high fat, low carb diet may not only be best for weight loss, but also for reducing several markers of cardiovascular risk in the obese. In short, as Dr Eenfeldt told the conference, ‘You don’t get fat from eating fatty foods just as you don’t turn green from eating green vegetables.’

This, of course, is a difficult message for many to swallow; particularly for heart patients, most of whom have spent years pursuing a low fat, low cholesterol diet as the best way to preserve heart health.

It’s a public health message that was first promoted in the sixties, after the globally respected Framingham Heart study sanctified high cholesterol as a major risk factor for heart disease. It’s a cornerstone of government and public health messages – yet what people didn’t know was that the study also threw up some more complex statistics. Like this one: for every 1mg/dl per year drop in cholesterol levels in those who took part in the study there was a 14% increase in cardiovascular death and an 11% increase in mortality in the following 18 years for those aged over 50.

It’s not the only statistic that doesn’t sit with the prevailing anti-cholesterol message: in 2013, a group of academics studied previously unpublished data from a seminal study done in the early seventies, known as the Sydney Diet Heart study. They discovered that cardiac patients who replaced butter with margarine had an increased mortality, despite a 13% reduction in total cholesterol. And the Honolulu heart study published in the Lancet in 2001 concluded that in the over-sixties a high total cholesterol is inversely associated with risk of death. Startling, isn’t it? A lower cholesterol is not in itself the mark of success, it only works in parallel with other important markers, like a shrinking waist size and diminishing blood markers for diabetes.

Conversely, a mounting slew of evidence suggests that far from contributing to heart problems, having full fat dairy in your diet may actually protect you from heart disease and type 2 diabetes. What most people fail to understand is that, when it comes to diet, it’s the polyphenols and omega 3 fatty acids abundant in extra virgin olive oil, nuts, fatty fish and vegetables that help to rapidly reduce thrombosis and inflammation independent of changes in cholesterol. Yet full fat dairy has remained demonized – until now.

In 2014, two Cambridge Medical Research Council studies concluded that the saturated fats in the blood stream that came from dairy products were inversely associated with Type 2 diabetes and heart disease. Meaning that in moderate amounts – no-one is talking about devouring a cheese board in one sitting here – cheese is actually a proponent of good health and longevity. The same study, incidentally, found that the consumption of starch, sugar and alcohol encourages the production of fatty acids made by the liver that correlate with an increased risk of these killer diseases.

It is around type 2 Diabetes, in fact, that the anti-fat pro-carb message of recent decades has done some of the greatest damage. A lot of patients suffering from Type 2 Diabetes – the most common kind – are laboring under the dangerous misapprehension that a low fat, starchy carbohydrate fuelled diet will help their medication work most effectively. They couldn’t be more wrong. Earlier this year, a critical review in the respected journal Nutrition concluded that dietary carbohydrate restriction is one of the most effective interventions for reducing features of metabolic syndrome. 

It would be better to rename type 2 diabetes “carbohydrate intolerance disease”. Try telling this to the public though. Like the man who called into a national radio show in Cape Town on which I was taking part to discuss the relationship between diet and heart disease. Diagnosed with Type 2 diabetes, he was under the impression he had to consume sugar so his diabetes medications could ‘work’ – when in fact it was going to worsen his symptoms. And how many doctors and patients know that although some of these medications to control blood sugar may marginally reduce the risk of developing kidney disease, eye disease and neuropathy, they don’t actually have any impact on heart attack, stroke risk or reduce death rates? On the contrary dangerously low blood sugar from overmedicating on diabetes drugs has been responsible for approximately 100,000 emergency room visits per year in the United States. 

(Related: is the new sugar tax going to help save lives?)

But who can blame the public for such misguided perceptions? In my opinion a perfect storm of biased research funding, biased reporting in the media and commercial conflicts of interest have contributed to an epidemic of misinformed doctors and misinformed patients. The result is a nation of over-medicated sugar addicts who are eating and pill-popping their way to years of misery with chronic debilitating diseases and an early grave.

It’s why, these days, I very seldom touch bread, have got rid of all added sugars and have embraced full fat as part of my varied Mediterranean-inspired diet. I feel better, have more energy and – even though I didn’t set out to do so – I’ve lost that fatty tyre around my waist, despite reducing the time I spend exercising.

Perhaps you can’t face making all those changes in one go. In which case, if you do one thing, make it this: next time you are in the supermarket and are tempted to pick up a pack of low-fat spread, buy a pack of butter instead or, better still, a bottle of extra virgin olive oil. Your heart will thank you for it. The father of modern medicine Hippocrates once said, “let food be thy medicine and medicine be thy food”. It’s now time we let “fat” be that medicine.

Dr Aseem Malhotra is a cardiologist, founding member of the Public Health Collaboration and advisor to the National Obesity Forum. 

The Fats You Don't Need to Fear, and the Carbs That You Do

The Fats You Don't Need to Fear, and the Carbs That You Do

By

Jane E. Brody

October 19, 2015 5:45 am October 19, 2015 5:45 am

Photo

Credit Paul Rogers

The nutritional pickle so many Americans are now in is largely a result of “an oversimplification of dietary recommendations that created a fat phobia,” Dr. Frank B. Hu of the Harvard T. H. Chan School of Public Health told me.

Starting in the 1970s, when accumulating evidence from animal and human studies showed that a diet high in saturated fats and cholesterol was an important risk factor for cardiovascular disease, dietary guidelines urged people to eat less fat.

Although health advice focused on saturated fats from high-fat animal foods, many people generalized the advice to mean all fats, choosing in their stead a panoply of reduced-fat and fat-free foods rich in carbohydrates, from crackers to sweetened yogurts. They especially increased their consumption of two kinds of carbohydrates, refined starches and sugars, that have helped to spawn the current epidemic of obesity and Type 2 diabetes.

Experts now realize that efforts to correct past dietary sins that made heart disease and stroke runaway killers have caused the pendulum to swing too far in the wrong direction.

“The mistake made in earlier dietary guidelines was an emphasis on low-fat without emphasizing the quality of carbohydrates, creating the impression that all fats are bad and all carbs are good,” Dr. Hu, a professor of nutrition and epidemiology, said. “It’s really important to distinguish between healthy fats and bad fats, healthy carbs and bad carbs.”

He explained that saturated fat, found in fatty animal foods like meats and dairy products, raises blood levels of cholesterol and is not healthy, “but olive oil is important — it’s beneficial for cardiovascular health and body weight.” Olive oil, like canola, avocado and nut oils, is monounsaturated, and while it has as many calories as meat and dairy fat, it does not raise serum cholesterol or foster fat-clogging deposits in blood vessels.

“We have to get out of the fat phobia mind-set,” Dr. Hu stressed, adding that we also have to abandon the idea that all complex carbohydrates are good.

Sugars are simple carbohydrates and starches are complex carbohydrates; all are ultimately broken down into glucose, the body fuel that circulates in blood. Sugars are digested rapidly, quickly raising blood glucose, but most starches take longer to digest.

Important exceptions are refined carbohydrates, like white bread and white rice. Starchy foods with highly processed grains that have been stripped of dietary fiber act more like sugar in the body. They are rapidly digested and absorbed, raising blood levels of glucose and prompting the secretion of insulin to process it. When consumed in excess of the body’s need for immediate and stored energy, refined carbs and sugars can result in insulin resistance and contribute to fatty liver disease.

Alas, potatoes, the nation’s most popular vegetable, act like sugars and refined carbohydrates. They have what is called a high glycemic index, the ability to raise blood glucose rapidly. Potatoes, Dr. Hu explained, are made of long chains of glucose easily digested by enzymes in the mouth and stomach, and the fat in French fries slows the process only slightly.

The concept of a glycemic index, proposed in 1981 by David Jenkins and his colleagues in The American Journal of Clinical Nutrition, has since been validated repeatedly and is now accepted as a good way to distinguish between the kinds of carbohydrates that are health-promoting or at least neutral and those that have negative health effects.

In 2002, Dr. David S. Ludwig, a pediatrician, endocrinologist and nutrition researcher at Boston Children’s Hospital and professor at the Harvard T. H. Chan School of Public Health, published a comprehensive review of how glycemic index influences human physiology, clearly demonstrating its importance to preventing and treating obesity, diabetes and cardiovascular disease. Had Americans and their physicians heeded it then, we might have been largely spared the fix we’re now in.

The index was developed by testing the glucose response to a standard amount of carbohydrate against a reference food, either pure glucose (index number 100) or white bread (71). High-glycemic foods like baked Russet potatoes (111), white baguette (95), cornflakes (93), white rice (89), pretzels (83), instant oatmeal (83), rice cakes (82), Gatorade (78) and French fries (75) induce higher blood glucose levels than ordinary white bread and are best consumed infrequently and in small quantities.

At the other end of the glycemic spectrum, oatmeal (55), pasta (46 for spaghetti, 32 for fettuccine), apples (39), carrots (35), skim milk (32), black beans (30), lentils (29), prunes (29), barley (28), chickpeas (10), grapefruit (25), peanuts (7) and hummus (6) have a smaller effect on blood glucose, and green vegetables like broccoli have too little an effect to be measured.

Closely related to the glycemic index is the glycemic load. While the glycemic index measures how quickly a particular food raises blood sugar, the glycemic load takes portion sizes into account. Hence a food like watermelon, with a high glycemic index, has a low glycemic load, since much of the fruit is water.

High-glycemic foods are a particular problem for people trying to control their weight. The amount of insulin released to lower blood glucose can overshoot the mark and result in a rapid return of hunger. A low-glycemic food, on the other hand, has no such effect. And those that are rich in wholesome fats, like peanuts or avocado, can actually delay the return of hunger, though the calories can add up quickly if consumed to excess.

“The glycemic index and glycemic load of the average diet in the United States appear to have risen in recent years because of increases in carbohydrate consumption and changes in food-processing technology,” Dr. Ludwig wrote in 2002. The pattern persisted in the decade that followed, and can largely explain the rise in overweight and obesity among Americans of all ages.

In addition, chronic consumption of meals with a high-glycemic effect can induce insulin resistance, the hallmark of Type 2 diabetes, and an excess of free fatty acids in the blood, resulting in fatty liver disease. The prevalence of both these disorders has risen in recent years, and both can lead to chronic inflammation, a promoter of cardiovascular disease.

Dr. Hu said that when he was growing up in China, most people were physically active and thus able to handle the glycemic load of large amounts of white rice consumed. “Now, however, the Chinese have become more sedentary but still consume large amounts of white rice, and both obesity and diabetes are on the rise,” he said.

This is What Happens to Your Body When You Eat Sugar

This is What Happens to Your Body When You Eat Sugar

By David Zinczenko with Stephen Perrine

Here’s a quick question: How many spoonfuls of high-fructose corn syrup did you eat yesterday?

Oh, you don’t recall slurping down any of the hyper-sweet corn extract? Well, you did—about eight teaspoons’ worth, according to the U.S. Department of Agriculture. In fact, the average American consumed 27 pounds of the stuff last year.

But while 8 teaspoons of artificially manufactured syrup may seem like an awful lot, it’s only a drop in the sugar bucket. The USDA’s most recent figures find that Americans consume, on average, about 32 teaspoons of added sugar every single day. That sugar comes to us in the form of candies, ice cream and other desserts, yes. But the most troubling sugar of all isn’t the added sugar we consume on purpose; it’s the stuff we don’t even know we’re eating.

In recent years, the medical community has begun to coalesce around a powerful new way of looking at added sugar: as perhaps the number one most significant health threat in America. But what exactly is “added sugar,” and why do experts suddenly believe that it’s the Freddy Kreuger of nutrition? Read on to find out—and to lose weight fast, read these essential 

The Deal with added sugar

When they talk about “added sugar,” health experts aren’t talking about the stuff that we consume from eating whole foods. “Added sugars are sugars that are contributed during the processing or preparation of foods and beverages,” says Rachel K. Johnson, PhD, RD, professor of nutrition at The University of Vermont. So lactose, the sugar naturally found in milk and dairy products, and naturally occurring fructose, the sugar that appears in fruit, don’t count. But ingredients that are used in foods to provide added sweetness and calories, from the much-maligned high fructose corn syrup to healthier-sounding ones like agave, date syrup, cane sugar, and honey, are all considered added sugars.

That’s because naturally occurring sugars, like what you find in an apple, come with their own health posse—fiber, which slows the digestion of the sugar and prevents it from spiking insulin response and damaging your liver, two serious side effects of added sugar. “It’s almost impossible to over-consume fructose by eating too much fruit,” says Johnson. Consider this: You’d need to eat six cups of strawberries to get the same amount of fructose as in one can of Coke.

Fortunately, giving up added sugar has been shown to have several dramatic and rapid impacts on your health. In a newly released study, children who cut added sugars from their diets for just 9 days showed dramatic improvements in cholesterol and blood sugar levels.

On the flip side, adding sugar to your diet can quickly put your health into a spiral: People who consumed beverages containing high fructose corn syrup for two weeks significantly increased their levels of triglycerides and LDL cholesterol (the “bad” cholesterols), plus two proteins associated with elevated cholesterols and another compound, uric acid, that’s associated with diabetes and gout. So found a 2015 study in the American Journal of Clinical Nutrition.

In fact, in a 2014 editorial in the journal JAMA Internal Medicine, the authors made a bold statement: “Too much sugar does not just make us fat; it can also make us sick.”

The editors of Eat This, Not That! took a look at the most recent research and discovered just how much harm added sugars are doing to us:

Added sugar makes eating healthy almost impossible. Read on to find out what it does to your body—and learn from this list of 

How a sugar rush works

The more added sugar that sneaks its way into your diet, the less healthy food you’ll eat the rest of the day. That’s the finding of a 2015 article in Nutrition Review, which looked at dozens of studies conducted between 1972 and 2012. The researchers found that a higher intake of added sugar was associated with poorer diet and a lower intake of micronutrients.

That’s in part because of how sugary foods retrain our taste buds and mess with our bodily systems. When even tomato sauce is laced with sweetener, we then need greater and greater doses of sugar in order for the flavor to register. That leads us to seek out candies and baked goods at the expense of real food.

But it’s not just a matter of taste. A sugar rush creates an overflow of insulin into the system to try to manage the toxic substance. Because it can create an overreaction within the body—too much insulin pulling too much sugar out of the bloodstream—it can lead to crash that sends us seeking another immediate sugar rush, the kind that no whole food can satisfy.

The most powerful effects, however, aren’t on our bodies. They’re on our brains. In one study, researchers measured the levels of oxytocin, a feel-good hormone that helps us feel satiated, in the brains of rats. When rats that ate a low-sugar diet were given a meal high in sugar, their oxytocin levels didn’t change. But when they were given the high-sugar diet regularly, their brains began to show lower levels of oxytocin activity. In other words, the more we’re bombarded with added sugars, the more chronically unsatisfied we feel, and the more we need to eat. An editorial in JAMA Internal Medicine asked, “Why are we consuming so much sugar despite knowing too much can harm us?” The answer: “The high prevalence of added-sugar consumption…is very likely influenced by and a result of addictive behaviors incited by reward system activation after overeating highly palatable foods.” (For more shocking calorie bombs you’re probably eating, click here for the 

Added sugar causes your body to store fat around your belly

Within 24 hours of eating fructose, your body is flooded with elevated levels of triglycerides. Does that sound bad? It is.

Triglycerides are the fatty deposits in your blood. Your liver makes them, because they’re essential for building and repairing the tissues in your body. But when it’s hit with high doses of fructose, the liver responds by pumping out more triglycerides; that’s a signal to your body that it’s time to store some abdominal fat. In one study, researchers fed subjects beverages sweetened with either glucose or fructose. Both gained the same amount of weight over the next 8 weeks, but the fructose group gained its weight primarily as belly fat, thanks to the way this type of sugar is processed in the liver.

What’s unique to fructose is that it seems to be a universal obesogen—in other words, every creature that eats it gains weight. Princeton researchers recently found that high-fructose corn syrup seemed to have a unique impact on weight in their animal studies. “When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they’re becoming obese—every single one, across the board,” psychology professor Bart Hoebel, a specialist in appetite and sugar addiction, said in a report from the university. “Even when rats are fed a high-fat diet, you don’t see this; they don’t all gain weight.” Fructose is the freak show of fat. (If you’re genuinely hungry, turn to one of the rather than filling up on candy.)

Added sugar makes you skip going to the gym

There are a lot of ways that added sugar can make you gain weight, but the most bizarre may be the way it reduces actual physical activity. In one study at the University of Illinois, mice that were fed a diet that mimicked the standard American diet–i.e., one that was about 18 percent added sugars—gained more body fat even though they weren’t fed more calories. One of the reasons was that the sugar-addled mice traveled about 20 percent less in their little cages than mice that weren’t fed the sugary diet. They just naturally…slowed…down.

Added sugar is the number one factor in your risk of dying from diabetes

The link between increased sugar and diabetes risk is right up there with “smoking causes lung cancer” on the list of immutable medical truths— despite what soda manufacturers are trying to tell us. (You’ll read more about sugar-based hocus-pocus in the next chapter.) But researchers at the Mayo Clinic have come right out and said that added fructose—either as a constituent of table sugar or as the main component of high-fructose corn syrup—may be the number one cause of diabetes, and that cutting sugar alone could translate into a reduced number of diabetes deaths the world over.

Added sugar makes you dumb, demented, and depressed

“Reduce fructose in your diet if you want to protect your brain,” announced Fernando Gomez-Pinilla, professor at the University of California Los Angeles. He and his team tested how well rats recovering from brain injury learned new ways to get through a maze. They found that animals that drank HFCS took 30 percent more time to find the exit. “Our findings suggest that fructose disrupts plasticity — the creation of fresh pathways between brain cells that occurs when we learn or experience something new,” he says.

In an earlier study, researchers found that a combination of sugar and fat could actually change one’s brain chemistry. The brains of animals on a high-fat, high-sugar diet had decreased levels of BDNF, a compound that helps brain cells communicate with one another, build memories, and learn new things; decreased levels of BDNF have been linked to both Alzheimer’s and depression.

One of the recent mysteries of science is why depression, diabetes and dementia seem to cluster in epidemiological studies, and why having one of these health issues seems to increase your risk for the others. The answer: In a study in the journal Diabetologia, researchers found that when blood glucose levels are elevated, BDNF levels drop. That means that the simple act of eating sugar makes you instantly dumber; the more you do it, the greater your risk of diabetes, and the greater your risk of depression and dementia as well. In a 2015 study of post-menopausal women, higher levels of added sugars and refined carbs were associated with an increased likelihood of depression, while higher consumption of fiber, dairy, fruit and vegetables was associated with a lower risk.

And, in a study of nearly 1,000 seniors (median age: 79.5), researchers found that eating a diet high in simple carbs significantly increased the risk of developing dementia. All of the subjects were cognitively normal at the beginning of the study, and about 200 developed signs of dementia over the next 3.7 years. The risk of mental decline was higher in those who ate high-carb diets, and lower in those whose diets were higher in fat and/or protein. (Speaking of sugar, don’t miss our ultimate list of the 

Sugar doubles your risk of dying from heart disease

People who get 25 percent of more of their calories from added sugar are more than twice as likely to die from heart disease as those who eat less than 10 percent, according to a study in the Journal of the American Medical Association. One out of ten of us fall into that category.

Now, if you’re an average American, your daily sugar consumption is about 17 percent of calories, according to the study. But that’s hardly a laurel to rest on. People who ate between 17 and 21 percent of their calories from added sugar had a 38 percent higher risk of dying from heart disease, compared with people who consumed 8 percent or less of their calories from added sugar.

At first, the researchers figured that since those who ingest more sugar have poorer diets, that might be a main cause. But even after making adjustments for the quality of one’s diet, the link between sweets and cardiovascular risk remained the same.

The study found that the major sources of added sugar in the American diet were:

• Sugar-sweetened beverages (37.1%)
• Grain-based desserts like cookies or cake (13.7%)
• Fruit drinks (8.9%)
• Dairy desserts like ice cream (6.1%)
• Candy (5.8%)

And sodas and other sweet drinks are a major red flag: The researchers found that a higher consumption of sugar-sweetened beverages was directly tied to an increased risk of dying from heart disease. The impact is so great that you don’t need to be meandering through middle age to see the impact: Even teenagers who consume food and beverages high in added sugars show evidence of risk factors for heart disease and diabetes in their blood, according to a second study in The Journal of Nutrition. (For decadent fat-burners, don’t miss this list of the 25 Best Carbs That Uncover Your Abs!)

Added sugar raises your blood pressure

In fact, sugar may be worse for your blood pressure than salt, according to a paper published in the journal Open Heart. Just a few weeks on a high-sucrose diet can increase both systolic and diastolic blood pressure. Another study found that for every sugar-sweetened beverage, risk of developing hypertension increased 8 percent. Too much sugar leads to higher insulin levels, which in turn activate the sympathetic nervous system and lead to increased blood pressure, according to James J. DiNicolantonio, PharmD, cardiovascular research scientist at Saint Luke’s Mid America Heart Institute in Kansas City, Missouri. “It may also cause sodium to accumulate within the cell, causing calcium to build up within the cell, leading to vasoconstriction and hypertension,” he says.

Sugar causes your skin to sag

Your skin has its own support system in the form of collagen and elastin, two compounds that keep your skin tight and plump. But when elevated levels of glucose and fructose enter the body, they link to the amino acids present in the collagen and elastin, producing advanced glycation end products, or “AGEs.” That damages these two critical compounds and makes it hard for the body to repair them. This process is accelerated in the skin when sugar is elevated, and further stimulated by ultraviolet light, according to a study in Clinical Dermatology. In other words, eating lots of sugar poolside is the worst thing you can do for your skin.

More from Eat This, Not That!

All You Wanted to Know About Diabetes and Alcohol but Were Embarrassed to Ask

All You Wanted to Know About Diabetes and Alcohol but Were Embarrassed to Ask

Siva Vallabhaneni March 23, 2015

Can diabetics have alcohol? If yes, how much is safe? Can heavy drinking lead to diabetes?

This article will try to answer common questions about diabetes and alcohol.

Can heavy drinking lead to diabetes?

Yes it can. Heavy drinking reduces insulin sensitivity. If you’re a heavy drinker, you are also amassing huge amount of calories. For example, a pint of lager beer contains as many calories as a slice of pizza. Too many calories inevitably result in weight gain. Obesity has been linked to insulin resistance and insulin resistance is the stepping stone to type 2 diabetes.

Heavy drinking also causes pancreatitis – the inflammation of pancreas. Most heavy drinkers report shooting pain in the upper abdomen, nausea – sometimes during eating, and vomiting. These are the symptoms of a swollen pancreas. Pancreatitis can lead to type 2 diabetes.

I’m a Teetotaler, what’s my risk?

Crazy as it sounds, drinking in moderation can actually prevent type 2 diabetes. That’s unfair to teetotalers but true. There is only one explanation for that. When you are drinking, your liver drops all other activity and just focuses on breaking down the alcohol. While your liver is doing that, the blood glucose levels drop, but not dangerously in a normal, healthy person.

Over a period of time, drinking in moderation can actually improve insulin sensitivity. We’re not lying. A review of 15 studies found that moderate drinkers were at lower risk of diabetes than teetotalers and heavy drinkers.

What is drinking in moderation? 

Good question. If you’re a woman, you shouldn’t drink more than three units a day. If you’re a man, stop at fourth unit. But what is a unit?

One unit of alcohol is 10 ml of pure alcohol. But you don’t drink pure alcohol – you drink beer, wine or bourbon, rum, or whisky. So how can you know how many units are there in a pint of lager? Here’s a guide:

1. One pint of lager – 2 units
2. A shot (25ml) of hard spirits (whisky, rum, or vodka) – 1 unit
3. A glass of wine (125ml) – 1.5 units

It takes an average person about an hour to breakdown a unit of alcohol. The processing times varies according to gender, age, weight, height, among others. The more you drink, longer it will take your body to process it.

Can a diabetic have alcohol?

No two cases of diabetes are alike. Some diabetics can enjoy alcohol in moderation while to others it could be life-threatening. There is scientific evidence that shows that consuming alcohol may reduce your chances of following to a diet plan, exercise routine or medication regimen. Consuming alcohol also raises blood pressure which may worsen some complications such as neuropathy, retinopathy.

Diabetes and alcohol are uneasy bedfellows. That said, some diabetics can have alcohol in moderation, but it pays to follow some guidelines, such as:

Consult your doctor: If there’s a social call where you know drinks will be served, tell your doctor about it. Your doctor is the best judge to determine whether or not alcohol will interfere with your medication. If you take insulin shots or other medicines, consuming alcohol can make your blood sugar dangerously low. The chances of hypoglycemia are very real.

Declare your diabetic-status – There is a blurred line between signs of hypoglycemia and being inebriated. If you’re drinking in a public event, make sure you inform couple of people that you have diabetes and if you pass out, it could be due to hypoglycemia and you might need medical attention. We know it’s uncool, but necessary.

Check blood sugar before and after the drink – Monitoring your blood sugar can prevent unfortunate incidence of hitting a low. Most importantly, you should check your blood sugar before sleeping. If it’s under 100 mg/dl, make sure you eat something to avoid hypoglycemia during the sleep.

Never drink on empty stomach or after exercise – It is important to have normal blood sugar levels before drinking. Food also slows down the absorption of alcohol. Keep eating snacks with your drink. It is a good idea to drink really slowly. Drinking slow reduces the pressure on your liver. Never drink immediately after exercising as your blood sugar levels are usually low after exercising.

Watch the Calories – Is that JD with coke? Is that cocktail loaded with sugar syrup and artificial juice?  Watch out for empty calories. Keep hydrated while you’re drinking. Keep water handy.