Wellness

[cherry]

Carbs May Be Intrinsically Bad, Regardless of Weight

F. Perry Wilson, MD, MSCE

Disclosures

June 26, 2019

Welcome to Impact Factor, your weekly portion of commentary on a new medical study. I'm Dr F. Perry Wilson.

This week , another nail in the carbohydrate coffin as a small but rigorous study appearing in JCI Insight suggests that a low-carb, high-fat diet improves the metabolic syndromeeven when weight doesn't change.[1]

A quick reminder: Metabolic syndrome is defined as having at least three of the five factors on this list.

 

These factors seem to be tied to insulin resistance, so avoiding insulin secretion (by limiting carb intake) has always made sense. Indeed, prior studies of low-carb diets have shown improvements in metabolic syndrome parameters, but those diets were also associated with weight loss, which led to a big question: Are low-carb diets beneficial because they help people lose weight or because there is something intrinsically bad about carbs themselves?

The JCI Insight paper finally gives us the answer, and the carb producers of the world aren't going to like it.

This was a physiologic study; 16 individuals were randomized to three different diets for 4-week periods.

 

Each individual randomly received either a low-carb diet, a moderate-carb diet, or a high-carb diet. Protein levels were fixed, so think of low-carb and high-fat as synonymous here. Each participant received each diet with 2-week washouts in between. They thus served as their own control—a smart design choice in a small study like this. Critically, the diets were designed to have a total caloric content that would not lead to weight changes. This was not a weight-loss intervention; it was a pure dietary change intervention.

After each 4-week diet, researchers measured a slew of biochemical parameters, and the tale of the tape was quite telling.

 

Looking at those metabolic syndrome parameters, there was no significant change in waist circumference or blood pressure, but fasting glucose levels and triglycerides were significantly lower in the low-carb diet group, while HDL was higher.

In fact, of the 16 individuals in the trial, nine no longer met criteria for metabolic syndrome after 4 weeks of the low-carb diet. By comparison, only one individual no longer met the definition of metabolic syndrome after 4 weeks of the high-carb diet.

 

Other surprising findings: Blood levels of saturated fats were actually lower in the low-carb group, which had a substantially higher saturated fat intake (mostly in the form of cheese). This argues that the old canard "You are what you eat" doesn't quite jibe with modern metabolic science.

 

Over the past five decades, carbohydrate consumption among Americans has skyrocketed, and rates of metabolic syndrome along with it. This study is the best so far to suggest that this relationship is not just driven by increases in weight but by the carbs themselves. The long-running war on fat may turn out to be a case of friendly fire.

[cherry]

Researchers find protein that might prevent, reverse diabetes

Published Saturday 22 June 2019

By Tim Newman

Fact checked by Gianna D'Emilio

A recent study finds that targeting a specific protein within the fat cells of mice reverses type 2 diabetes. The results also show that the protein can prevent the disease from developing.

Could new findings lead the way to improved diabetes treatments?

Since the 1980s, the global prevalence of diabetes has almost quadrupled.

According to the Centers for Disease Control and Prevention (CDC), in the United States, around 1 in 10 people have type 2 diabetes (T2D), the most common form of diabetes.

A further 1 in 3 people has prediabetes — higher-than-normal blood sugar levels that increase the risk of T2D.

The steady rise in levels of T2D is largely due to the increase in obesity rates: Obesity is one of the primary risk factors for diabetes.

Insulin is a hormone that regulates the levels of sugar in the blood. In T2D, the body either does not respond to the hormone, or it does not produce enough of it.

Although medications and lifestyle changes can help to manage insulin levels and control diabetes, there is no cure, and researchers are keen to find better interventions.

Recently, a group of researchers — many of whom are from the University of British Columbia, in Canada, or the Karolinska Institute, in Sweden — examined the role of a specific protein in fat cells.

They recently published their findings in the journal EBioMedicine.

White adipose tissue

When we eat more calories than our body needs, a type of fat called white adipose tissue (WAT) expands to store the excess energy as fat. However, if we take on more energy than we need for more extended periods, this system cannot cope, eventually leading to insulin resistance.

In particular, the researchers were interested in how a glycoprotein called CD248 might influence WAT and the eventual development of T2D.

Researchers have previously associated CD248 with tumor growth and inflammation, but no one had investigated its role in T2D.

First, the researchers analyzed the gene expression in WAT from humans who were thin, obese, had T2D, or did not have T2D.

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In those who had obesity or were insulin resistant, they found that the CD248 gene was upregulated; in other words, the body was making more of the protein. This observation led the scientists to conclude that CD248 might work as a marker of insulin sensitivity that is more sensitive than current methods.

Next, the researchers artificially reduced the activity of CD248 in human WAT cells in the laboratory.

From these experiments, they concluded that CD248 in WAT plays a role in the cellular processes that lead to insulin resistance caused by long-term overconsumption of energy. Specifically, they found that CD248 is involved in how cells respond to hypoxia, which is a hallmark of obesity.

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Moving to a mouse model

Then, the scientists moved to a mouse model. They used mice that lacked the gene that codes for CD248 in their WAT (although other cell types were still producing CD248). In these experiments, the researchers found that the mice were protected from developing insulin resistance and T2D.

The mice did not develop diabetes, even when they were fed a high-fat diet and became obese.

Importantly, the mice with reduced CD248 in their fat cells did not appear to experience any adverse events, suggesting that targeting this protein might be a useful therapy in the future.

Aside from the protective effects of reducing CD248, the scientists also demonstrated its potential as a therapy for those who already have T2D.

"A most interesting finding was that the insulin sensitivity of mice that already have diabetes can be improved by reducing CD248 levels in the fat cells, even while they remain obese."

Co-senior author Dr. Edward Conway

Early days

Although these findings are fascinating and add to our understanding of how T2D develops, researchers will need to conduct a great deal of work before the results can make their way to the pharmacy.

Dr. Conway adds a note of caution, "While these discoveries are exciting, we are still some distance from a new treatment." However, he plans to continue his investigations, explaining, "Our immediate goals are to understand how CD248 works so that safe and effective drugs that reduce the protein's levels or that interfere with its function can be designed."

The journey from research in cells and mice to treating human patients is a long, expensive, and often unsuccessful one.

The study suggests a new way to assess insulin resistance, prevent its progression, and even reverse T2D. Because diabetes is advancing at a worrying rate, chasing up these leads is now urgent.

[Laura14]

How cool is that @cherry !   

That first study is confirming what some of the brain researchers are finding.  And I about did a happy dance when they said cheese was a non issue which it probably wouldn't be with diabetes since it's a fat. 

Not sure that would work with APOE4 peeps (huge no no with the brain guys) although I did find one who said sparingly is not going to hurt you.  The other said it's APOE4's kryptonite and he can tell an APOE4 just from their food diaries.  Cheese is always in the top 3.  LOL   

Specific to diabetes, this just makes sense though.  Glad they are finding some science to back them up and hopefully find a way to resensitize the cells again.  It's about time our generation cured something already.      

[cherry]

@Laura14  I went through lent eating Mac and cheese made with resistant starch macaroni. I never had 1 sugar spike, and they had changed my medication from Metformin, to Januvia, and I am taking less  than the metformin dose

Cheese didn't spike my sugar ,nor did the pasta, after cooling it overnight, before I baked ..it

[Laura14]

@cherry   It shouldn't.  Cheese is all fat.

[cherry]

It is dairy and there is sugar in milk @Laura..Some places warn you against  dairy

[Laura14]

I have never heard of sugar in cheese.  That's a new one on me unless the are counting natural sugars that may exist in the milk.  It's got to be way low even then.  You taught me something new @cherry .  Glad you are finding what works for you.  

[cherry]

Maybe it poured out with the whey, when it is  made @Laura14  Milk has lactose , which is sugar..Haven't you ever noticed that milk has a sweet taste to it?

It is carb ,and some people can't digest it properly..That is why they have special types of milk

[Laura14]

You would think the curdling process would dispense with most of it and I looked it up and it really does.  Very low sugar but there is some.  You are correct @cherry !

[cherry]

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

Image copyright Getty Images

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."