Type 2 Diabetes Could Be a Cause of Erectile Dysfunction


Type 2 diabetes may be a causal factor in the development of erectile dysfunction (ED), with insulin resistance a likely mediating pathway, results of a large-scale genomic analysis suggest. The data also uncovered a genetic locus linked to ED.

Jonas Bovijn, MD, DPhil, Big Data Institute at the University of Oxford, United Kingdom, and colleagues gathered data on more than 220,000 men across three cohorts, of whom more than 6000 had ED.

The researchers initially showed that a region on chromosome 6 is linked to the development of ED. The location suggested that the condition is associated with dysregulation of the hypothalamus.

Next, they performed a Mendelian randomization analysis, which examined the relationship between gene mutations known to be associated, in this case, with cardiometabolic factors and the outcome of ED.

The research, published online December 20 in the American Journal of Human Genetics, showed that a genetic predisposition to type 2 diabetes increased the risk for ED. The risk was driven primarily by susceptibility to insulin resistance.

Bovijn said in a release: “We know that there is observational evidence linking erectile dysfunction and type 2 diabetes, but until now there has not been definitive evidence to show that predisposition to type 2 diabetes causes erectile dysfunction.”

“Further research is needed to explore the extent to which drugs used in the treatment of type 2 diabetes might be repurposed for the treatment of ED,” the team notes.

Co–senior author Anna Murray, PhD, University of Exeter Medical School, United Kingdom, said in the release that “until now little has been known” about the cause of ED.

Previous studies have suggested there is a genetic basis for ED. The new study goes further by demonstrating that a genetic predisposition to type 2 diabetes is linked to ED, according to Murray.

“That may mean that if people can reduce their risk of diabetes through healthier lifestyles, they may also avoid developing erectile dysfunction,” she said.

Michael Holmes, MD, PhD, of the Nuffield Department of Population Health at the University of Oxford, who was one of the senior authors, agreed.

“Our finding is important, as diabetes is preventable, and indeed one can now achieve ‘remission’ from diabetes with weight loss, as illustrated in recent clinical trials.

“This goes beyond finding a genetic link to erectile dysfunction to a message that is of widespread relevance to the general public, especially considering the burgeoning prevalence of diabetes,” Holmes said.

Large Studies Key

Although the prevalence of ED is known to increase with age, rising to 20% to 40% among men aged 60 to 69 years, the genetic architecture of the condition remains poorly understood. This is at least in part due to a lack of well-powered studies.

The researchers therefore conducted a genome-wide association study (GWAS) using data on 199,362 individuals from the UK Biobank cohort and 16,787 people from the Estonian Genome Center of the University of Tartu (EGCUT) cohort, both of which are population based.

In addition, they included information on 7666 participants in the hospital-recruited Partners HealthCare Biobank (PHB) cohort.

The prevalence of ED, which was determined on the basis of self- or physician-reported ED, the use of oral ED medication, or a history of ED surgical intervention, was 1.53% in the UK Biobank, 7.04% in EGCUT, and 25.35% in PHB.

The researchers believe that the difference in prevalence rates between the cohorts may relate to the older average age for men in PHB, at 65 years, vs 59 years in the UK Biobank and 42 in EGCUT. In addition, the prevalence in the UK Biobank cohort may have been affected by a “healthy volunteer” selection bias and a lack of primary care data.

GWAS on the UK Biobank data indicated that there was a single genome-wide significant locus at 6q16.3 between the MCHR2 and SIM1 genes, with rs57989773 the lead variant.

Pooled meta-analysis of the combined cohorts indicated that rs57989773 was associated with ED at an odds ratio of 1.20 per C-allele (P = 5.71 × 10-14).

Synthesizing previous research on SIM1, which is highly expressed in the hypothalamus, in both human and rodent models, the team found that rs57989773 is associated with syncope, orthostatic hypotension, and urinary incontinence.

Moreover, the common risk variant for ED at 6q16.3 is linked to blood pressure and adiposity, as well as male sexual behavior in mice.

The researchers, therefore, suggest that a potential mechanism for the effect of the MCHR2-SIM1 locus on ED could be the hypothalamic dysregulation of SIM1.

The team also performed Mendelian randomization analyses to examine the potential causal role of cardiometabolic traits in ED risk.

Factors included type 2 diabetes, insulin resistance, systolic blood pressure (SBP), low-density lipoprotein (LDL) cholesterol levels, smoking heaviness, alcohol consumption, body mass index, coronary heart disease, and educational attainment.

The analysis revealed that type 2 diabetes was causally implicated in ED, with the risk for ED increased 1.11-fold with each 1-log higher genetic risk for type 2 diabetes (P = 3.5 × 10-4).

Insulin resistance was found to be a likely mediating pathway for the relationship, with an odds ratio for ED of 1.36 per 1 SD genetic increase in insulin resistance (P = .042).

SBP also had a causal effect on ED risk, at an odds ratio of 2.34 per 1 SD increase in SBP (P = .007).

LDL cholesterol was found to have a minor impact on the risk for ED, at an odds ratio of 1.07 per 1 SD increase in levels (P = .113). There was no association between ED and either smoking heaviness or alcohol use.

Source:Medscape.com

Type 2 Diabetes Could Be a Cause of Erectile Dysfunction


Type 2 diabetes may be a causal factor in the development of erectile dysfunction (ED), with insulin resistance a likely mediating pathway, results of a large-scale genomic analysis suggest. The data also uncovered a genetic locus linked to ED.

Jonas Bovijn, MD, DPhil, Big Data Institute at the University of Oxford, United Kingdom, and colleagues gathered data on more than 220,000 men across three cohorts, of whom more than 6000 had ED.

The researchers initially showed that a region on chromosome 6 is linked to the development of ED. The location suggested that the condition is associated with dysregulation of the hypothalamus.

Next, they performed a Mendelian randomization analysis, which examined the relationship between gene mutations known to be associated, in this case, with cardiometabolic factors and the outcome of ED.

The research, published online December 20 in the American Journal of Human Genetics, showed that a genetic predisposition to type 2 diabetes increased the risk for ED. The risk was driven primarily by susceptibility to insulin resistance.

Bovijn said in a release: “We know that there is observational evidence linking erectile dysfunction and type 2 diabetes, but until now there has not been definitive evidence to show that predisposition to type 2 diabetes causes erectile dysfunction.”

“Further research is needed to explore the extent to which drugs used in the treatment of type 2 diabetes might be repurposed for the treatment of ED,” the team notes.

Co–senior author Anna Murray, PhD, University of Exeter Medical School, United Kingdom, said in the release that “until now little has been known” about the cause of ED.

Previous studies have suggested there is a genetic basis for ED. The new study goes further by demonstrating that a genetic predisposition to type 2 diabetes is linked to ED, according to Murray.

“That may mean that if people can reduce their risk of diabetes through healthier lifestyles, they may also avoid developing erectile dysfunction,” she said.

Michael Holmes, MD, PhD, of the Nuffield Department of Population Health at the University of Oxford, who was one of the senior authors, agreed.

“Our finding is important, as diabetes is preventable, and indeed one can now achieve ‘remission’ from diabetes with weight loss, as illustrated in recent clinical trials.

“This goes beyond finding a genetic link to erectile dysfunction to a message that is of widespread relevance to the general public, especially considering the burgeoning prevalence of diabetes,” Holmes said.

Large Studies Key

Although the prevalence of ED is known to increase with age, rising to 20% to 40% among men aged 60 to 69 years, the genetic architecture of the condition remains poorly understood. This is at least in part due to a lack of well-powered studies.

The researchers therefore conducted a genome-wide association study (GWAS) using data on 199,362 individuals from the UK Biobank cohort and 16,787 people from the Estonian Genome Center of the University of Tartu (EGCUT) cohort, both of which are population based.

In addition, they included information on 7666 participants in the hospital-recruited Partners HealthCare Biobank (PHB) cohort.

The prevalence of ED, which was determined on the basis of self- or physician-reported ED, the use of oral ED medication, or a history of ED surgical intervention, was 1.53% in the UK Biobank, 7.04% in EGCUT, and 25.35% in PHB.

The researchers believe that the difference in prevalence rates between the cohorts may relate to the older average age for men in PHB, at 65 years, vs 59 years in the UK Biobank and 42 in EGCUT. In addition, the prevalence in the UK Biobank cohort may have been affected by a “healthy volunteer” selection bias and a lack of primary care data.

GWAS on the UK Biobank data indicated that there was a single genome-wide significant locus at 6q16.3 between the MCHR2 and SIM1 genes, with rs57989773 the lead variant.

Pooled meta-analysis of the combined cohorts indicated that rs57989773 was associated with ED at an odds ratio of 1.20 per C-allele (P = 5.71 × 10-14).

Synthesizing previous research on SIM1, which is highly expressed in the hypothalamus, in both human and rodent models, the team found that rs57989773 is associated with syncope, orthostatic hypotension, and urinary incontinence.

Moreover, the common risk variant for ED at 6q16.3 is linked to blood pressure and adiposity, as well as male sexual behavior in mice.

The researchers, therefore, suggest that a potential mechanism for the effect of the MCHR2-SIM1 locus on ED could be the hypothalamic dysregulation of SIM1.

The team also performed Mendelian randomization analyses to examine the potential causal role of cardiometabolic traits in ED risk.

Factors included type 2 diabetes, insulin resistance, systolic blood pressure (SBP), low-density lipoprotein (LDL) cholesterol levels, smoking heaviness, alcohol consumption, body mass index, coronary heart disease, and educational attainment.

The analysis revealed that type 2 diabetes was causally implicated in ED, with the risk for ED increased 1.11-fold with each 1-log higher genetic risk for type 2 diabetes (P = 3.5 × 10-4).

Insulin resistance was found to be a likely mediating pathway for the relationship, with an odds ratio for ED of 1.36 per 1 SD genetic increase in insulin resistance (P = .042).

SBP also had a causal effect on ED risk, at an odds ratio of 2.34 per 1 SD increase in SBP (P = .007).

LDL cholesterol was found to have a minor impact on the risk for ED, at an odds ratio of 1.07 per 1 SD increase in levels (P = .113). There was no association between ED and either smoking heaviness or alcohol use.

 

Source:Medscpe.com

People who drink moderate amounts of coffee each day have a lower risk of death from disease


Image: People who drink moderate amounts of coffee each day have a lower risk of death from disease

Many people drink coffee for an energy boost, but do you know that it can also prolong your life? A study published in the journal Circulation revealed that moderate amounts — or less than five cups — of coffee each day can lower your risk of death from many diseases, such as cardiovascular disease, Type 2 diabetes, and nervous system disorders. It can also lower death risk due to suicide.

The study’s researchers explained this effect could be attributed to coffee’s naturally occurring chemical compounds. These bioactive compounds reduce insulin resistance and systematic inflammation, which might be responsible for the association between coffee and mortality. (Related: Coffee drinkers have a lower mortality rate and lower risk of various cancers.)

The researchers reached this conclusion after analyzing the coffee consumption every four years of participants from three large studies: 74,890 women in the Nurses’ Health Study; 93,054 women in the Nurses’ Health Study 2; and 40,557 men in the Health Professionals Follow-up Study. They did this by using validated food questionnaires. During the follow-up period of up to 30 years, 19,524 women and 12,432 men died from different causes.

They found that people who often consumed coffee tend to smoke cigarettes and drink alcohol. To differentiate the effects of coffee from smoking, they carried out their analysis again among non-smokers. Through this, the protective benefits of coffee on deaths became even more apparent.

With these findings, the researchers suggested that regular intake of coffee could be included as part of a healthy, balanced diet. However, pregnant women and children should consider the potential high intake of caffeine from coffee or other drinks.

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Because the study was not designed to show a direct cause and effect relationship between coffee consumption and dying from illness, the researchers noted that the findings should be interpreted with caution. Still, this study contributes to the claim that moderate consumption of coffee offers health benefits.

The many benefits of coffee

Many studies have shown that drinking a cup of coffee provides health benefits. Here are some of them:

  • Coffee helps prevent diabetes: A study conducted by University of California, Los Angeles (UCLA) researchers showed that drinking coffee helps prevent Type 2 diabetes by increasing levels of the protein sex hormone-binding globulin (SHBG), which regulates hormones that influence the development of Type 2 diabetes. Researchers from Harvard School of Public Health (HSPH) also found that increased coffee intake may lower Type 2 diabetes risk.
  • Coffee protects against Parkinson’s disease: Studies have shown that consuming more coffee and caffeine may significantly lower the risk of Parkinson’s disease. It has also been reported that the caffeine content of coffee may help control movement in people with Parkinson’s disease.
  • Coffee keeps the liver healthy: Coffee has some protective effects on the liver. Studies have shown that regular intake of coffee can protect against liver diseases, such as primary sclerosing cholangitis (PSC) and cirrhosis of the liver, especially alcoholic cirrhosis. Drinking decaffeinated coffee also decreases liver enzyme levels. Research has also shown that coffee may help ward off cancer. A study by Italian researchers revealed that coffee intake cuts the risk of liver cancer by up to 40 percent. Moreover, some of the results indicate that drinking three cups of coffee a day may reduce liver cancer risk by more than 50 percent.
  • Coffee prevents heart disease: A study conducted by Beth Israel Deaconess Medical Center (BIDMC) and HSPC researchers showed that moderate coffee intake, or two European cups, each day prevents heart failure. Drinking four European cups a day can lower heart failure risk by 11 percent.

Type 2 Diabetes: Medical Groups Disagree on What Your A1c Goals Should Be


A1c goals for type 2 diabetes

The American College of Physicians (ACP) has written a guidance statement for providers to use when selecting targets for pharmacologic treatment of type 2 diabetes.

In other words, they share how aggressive clinicians should be when it comes to using medications to treat type 2 diabetes.

The American College of Physicians Guidance Statement

1: Clinicians should personalize goals for glycemic control in patients with type 2 diabetes on the basis of a discussion of benefits and harms of pharmacotherapy, patients’ preferences, patients’ general health and life expectancy, treatment burden, and costs of care.

2: Clinicians should aim to achieve an HbA1c level between 7% and 8% in most patients with type 2 diabetes.

3: Clinicians should consider deintensifying pharmacologic therapy in patients with type 2 diabetes who achieve HbA1c levels less than 6.5%.

4: Clinicians should treat patients with type 2 diabetes to minimize symptoms related to hyperglycemia and avoid targeting an HbA1c level in patients with a life expectancy less than 10 years due to advanced age (80 years or older), residence in a nursing home, or chronic conditions (such as dementia, cancer, end-stage kidney disease, or severe chronic obstructive pulmonary disease or congestive heart failure) because the harms outweigh the benefits in this population.

Diabetes Medical Associations Disagree

Medical associations whose focus is diabetes do not agree with the ACP’s guidance statement.

The president of the ACP, Dr. Jack Ende explained in a statement that “ACP’s analysis of the evidence behind existing guidelines found that treatment with drugs to targets of 7 percent or less compared to targets of about 8 percent did not reduce deaths or macrovascular complications such as heart attack or stroke but did result in substantial harms,”

“The evidence shows that for most people with type 2 diabetes, achieving an A1C between 7 percent and 8 percent will best balance long-term benefits with harms such as low blood sugar, medication burden, and costs,” he added.

Do These Recommendations Prioritize Individualized Care?

It’s reasonable to wonder that if taking medications is not a burden and costs are not an issue and low blood sugar risk is appropriately managed, is an A1c between 7 and 8 percent less desirable than one closer to non-diabetic levels? Type 2 diabetes is a serious disease and a 7% A1c would lead to its diagnosis, meaning that an A1c between 7 and 8 is not ideal for good health.

Yet, the reality is that these burdens do exist for a great many patients. The ACP seems to make the case that when burdens increase and patients do not reap additional health benefits in return, the extra medication intervention is not worthwhile but actually detrimental.

It makes sense to seek guidance from statistics. The problem is when these recommendations trump individualized care. It may make sense for one type 2 patient to keep a higher A1c level based on their unique circumstances but it would be an irresponsible measure for a provider not to share the risks of the higher A1c with any patient and leave them inadequately treated.

The ACP is not against a more ideal end result, however.

“Although ACP’s guidance statement focuses on drug therapy to control blood sugar, a lower treatment target is appropriate if it can be achieved with diet and lifestyle modifications such as exercise, dietary changes, and weight loss,” said Dr. Ende. Perhaps this signals a change in focus from aggressive drug therapy to lifestyle interventions or perhaps more of an an emphasis on a healthier balance between the two.

The American Diabetes Association’s chief medical officer Dr. William Cefalu told NPR News that they disagree with the ACP’s guidelines and stand by their own. He said that new drugs are effective in managing blood sugar and carry less risk for low blood sugar and some of them help lower body weight and improve cardiovascular risk factors–a win/win for patients who need to address all three common issues.

Former president of the American Association of Endocrinologists, Dr. George Grunberger told NPR that “The moment your glucose goes above normal, it’s incurring damage to the back of the eye, to kidneys and to nerves, especially in your feet,” and that he worries these guidelines will effectively tell physicians not to worry too much about their patients elevated A1c levels.

The Endocrine Society released a statement as well, sharing their strong disagreement with the ACP’s statement. They pointed out in a press release that the ACP’s “recommendations do not consider the positive legacy effects of intensive blood glucose control confirmed in multiple clinical trials, particularly for those newly diagnosed with type 2 diabetes, and, therefore, are not reflective of the long-term benefits of lower A1C targets.”

The recommendations might prove costly if physicians do not treat each individual on a case-by-case basis. Physicians and patients need to have very candid talks about what is desired because not all patients want or are capable of the same things.

So Who is Right?

The ACP has a point about how few benefits are often seen at various points of treatment which barely outweigh burdens incurred by type 2 diabetes patients who are treated aggressively with medications.

However, other medical associations who recommend getting A1c levels lower are also accurate in recommending for lower targets. Blood sugar levels above normal do indeed cause damage, even if only slightly elevated. Patients have a right to be aware of that fact and to get help from their provider in achieving normal blood sugar levels, if possible.

Should providers encourage normal blood sugars or should they follow their patient’s lead? The ACP’s stance suggests the patient needs to advocate for the best blood sugar outcomes they can get. Will this guidance statement lead patients to leave providers who want them to settle at higher A1c targets? Finding new providers is often more than an inconvenience. Will this stance ultimately help or hurt patients?

As studies indicate, the future points to more emphasis on lifestyle habits as well as better medications. It’s also likely that continuous glucose monitoring devices, known as CGM are going to be used more in type 2 diabetes and become powerful aids. An individual with type 2 diabetes using a CGM will be able to find out exactly what certain foods, stress, and exercise does to their blood sugar levels and be motivated to act accordingly.

Perhaps a good question to ask is what motivations do people with type 2 diabetes have to rely more on lifestyle interventions versus aggressive medication protocols?

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Two type 2 diabetes drugs linked to higher risk of heart disease


Two type 2 diabetes drugs linked to higher risk of heart disease

December 21, 2018, Northwestern University
Credit: CC0 Public Domain

Two drugs commonly prescribed to treat Type 2 diabetes carry a high risk of cardiovascular events such as heart attack, stroke, heart failure or amputation, according to a new Northwestern Medicine study.

“People should know if the medications they’re taking to treat their could lead to serious cardiovascular harm,” said lead author Dr. Matthew O’Brien, assistant professor of general internal medicine and geriatrics at Northwestern University Feinberg School of Medicine and a Northwestern Medicine physician.  “This calls for a in the treatment of Type 2 diabetes.”

The study will be published Dec. 21 in JAMA Network Open.

The two drugs—sulfonylureas and —are commonly prescribed to patients after they have taken metformin, a widely accepted initial Type 2 diabetes treatment, but need a second-line medication because metformin alone didn’t work or wasn’t tolerated.

This is the first study to compare how each of the six major second-line drugs impact cardiovascular outcomes in Type 2 diabetes patients taking a second diabetes medication.

Basal is engineered to release slowly over the course of the day, compared to the other type of insulin (prandial insulin), which is faster acting and intended to be taken before meals.

More than half of patients nationwide (60 percent) who need a second-line drug are prescribed one of these two drugs, the study found. Yet, patients who take one of these two drugs are more likely—36 percent more for sulfonylureas and twice as likely for basal insulin—to experience cardiovascular harm than those taking a newer class of diabetes drugs known as DPP-4 inhibitors, the authors report.

“According to our findings, we only have to prescribe basal insulin to 37 people over two years to observe one cardiovascular event, such as a , stroke, or amputation,” O’Brien said. “For sulfonylureas, that number was a bit higher—103 people. But when you apply these numbers to 30 million Americans with diabetes, this has staggering implications for how we may be harming many patients.”

Physicians should consider prescribing newer classes of antidiabetic medications, such as GLP-1 agonists (e.g. liraglutide), SGLT-2 inhibitors (e.g. empagliflozin)or DPP-4 inhibitors (e.g. sitagliptin), more routinely after metformin, rather than sulfonylureas or basal insulin, the study authors suggest.

These drugs, however, are more expensive than the sulfonylureas, which is the main reason they are not as commonly prescribed, O’Brien said.

“This should force providers to think about cardiovascular effects of these drugs early in the course of diabetes treatment, and shift prescribing patterns to newer drugs that have more favorable cardiovascular profiles,” O’Brien said.

This was an observational study using data from 132,737 patients with Type 2 diabetes who were starting second-line treatment. The scientists were, therefore, able to use real-world evidence that complements findings from previous randomized trials which studied only one active compared to placebo.

8 Reasons You’re Waking Up Mid-Sleep, and How to Fix Them


Talk about a rude awakening.
woman laying in bed at night on her cell phone

One minute you’re snoozing peacefully, the next you’re wide awake in the dead of night. Sound familiar? Unless you’re blessed enough to conk out like the most determined of logs, you may have experienced this form of sleeplessness before. Waking up during the night isn’t uncommon—a study of 8,937 people in Sleep Medicine estimates that about a third of American adults wake up in the night at least three times a week, and over 40 percent of that group might have trouble falling asleep again (this is sometimes referred to as sleep maintenance insomnia).

So, what’s causing you to wake up in the middle of the night, and how can you stop it from happening? Here are eight common reasons, plus what you can do to get a good night’s rest.

1. Your room is too hot, cold, noisy, or bright.

Your arousal threshold—meaning how easy it is for something to wake you up—varies depending on what sleep stage you’re in, Rita Aouad, M.D., a sleep medicine physician at The Ohio State University Wexner Medical Center, tells SELF.

When you sleep, your body cycles through different sleep stages: 1, 2, 3, 4, and rapid-eye movement (REM). (Some schools of thought lump together stages 3 and 4.) The first stage of sleep is the lightest, Dr. Aouad explains. That’s when you’re most likely to startle awake because a door slams, a passing car’s headlights shine into your window, or because of some other environmental factor like your room being too hot or cold.

Ideally, your room should be dark, comfortably cool, and quiet when you sleep. This might not all be under your control, but do what you can, like using earplugs and an eye mask to block out errant noise and light, or buying a fan if your room is stifling.

2. You have anxiety.

Anxiety can absolutely wake you up at night,” Nesochi Okeke-Igbokwe, M.D., a physician in New York, tells SELF. In fact, trouble sleeping is one of the most common symptoms of an anxiety disorder, according to the Mayo Clinic. That’s because you can experience anxiety-induced issues that are severe enough to rouse you, like a galloping heartbeat or nightmares.

“Additionally, there are people who may experience what are called nocturnal panic attacks, meaning they may have transient episodes of intense panic that wake them up from their slumber,” Dr. Okeke-Igbokwe says.

If your anxiety regularly wakes you up, Dr. Okeke-Igbokwe recommends mentioning it to your doctor, who should be able to help you get a handle on any underlying anxiety or panic disorder at play. Doing so may involve cognitive behavioral therapy, anti-anxiety medication, or a combination of the two. “Meditation and deep-breathing exercises can also sometimes alleviate symptoms in some people,” Dr. Okeke-Igbokwe says.

3. Your full bladder can’t wait until the morning.

Nocturia—a condition that’s generally viewed as getting up to pee at least once during the night, though some experts say that’s not often enough to qualify—appears to be fairly common. A study in the International Neurourology Journal found that out of the 856 people surveyed, around 23 percent of women and 29 percent of men experienced nocturia.

Causes of nocturia include drinking too much fluid before bedtime, urinary tract infections, and an overactive bladder, per the Cleveland Clinic. Untreated type 1 or type 2 diabetes may also be a factor; having too much sugar in your bloodstream forces your body to extract fluid from your tissues, making you thirsty and possibly prompting you to drink and pee more, according to the Mayo Clinic.

If cutting back on your evening fluid intake doesn’t reduce your number of nightly bathroom trips, consult a doctor for other possible explanations.

4. You had a couple of alcoholic drinks.

Sure, alcohol can make it easy to drift off—even when you’re, say, on a friend’s couch instead of tucked into your bed—but it also has a tendency to cause fitful sleep. This is because alcohol can play around with your sleep stages in various ways. For instance, it seems as though alcohol is associated with more stage 1 sleep than usual in the second half of the night. Remember, stage 1 sleep is the period in which you’re most likely to wake up due to environmental factors. So if you’re looking for quality, sleep-through-the-night rest, it’s worth taking a look at how much alcohol you’re consuming.

Everyone metabolizes alcohol differently depending on factors like genetics, diet, and body size. However, Alexea Gaffney Adams, M.D., a board-certified internist at Stony Brook Medicine, recommends that people stop drinking at least three hours before going to bed to give their bodies time to process the alcohol. Since drinking often happens at night, we realize that can be an optimistic time cushion. Based on your personal factors and how much you drank, you might not need that much. But having some kind of buffer—and drinking plenty of water so you’re more likely to booze in moderation—may prevent alcohol from interfering with your sleep.

Also, Dr. Gaffney Adams notes that drinking alcohol too soon before bed will make you need to pee, increasing the likelihood you’ll wake up in the night to use the bathroom. Double whammy, that one.

5. You’ve got sleep apnea.

If you find yourself jolting awake and feeling like you need to catch your breath, sleep apnea might be the culprit. This disorder slows and/or stops your breathing while you are asleep.

If you have obstructive sleep apnea, the muscles in your throat relax too much, which narrows your airway, causing your oxygen levels to drop, the Mayo Clinic explains. If you have central sleep apnea, your brain doesn’t send the right signals to the muscles controlling your breathing, again causing this potentially harmful drop in oxygen. Complex sleep apnea features characteristics of both conditions.

To diagnose sleep apnea, your doctor may have you do an overnight sleep study that monitors your breathing, according to the Mayo Clinic. The most common treatment for sleep apnea is a continuous positive airway pressure (CPAP) machine, which is basically a mask you wear during sleep to help keep your airways open, but your doctor can help you explore the alternatives if necessary.

6. You have an overactive thyroid gland.

“This gland controls the function of several other organs,” Dr. Gaffney Adams tells SELF. When it’s overactive (also called hyperthyroidism), it creates too much of the hormone thyroxine, which can have ripple effects on many different systems in your body, according to the Mayo Clinic. Common symptoms of an overactive thyroid include trouble sleeping, an increased heart rate, sweating (including at night), anxiety, tremors, and more.

Your primary care physician or an endocrinologist (a doctor specializing in hormones) can test your blood to evaluate your hormone levels. If you do have an overactive thyroid, your doctor can walk you through the potential ways of treating it, including medications to slow your thyroid’s hormone production and beta blockers to reduce symptoms like a wild heartbeat.

7. You ate right before bedtime, or you didn’t eat recently enough before you went to sleep.

“Eating too heavy of a meal too close to bedtime can make it difficult to fall asleep or stay asleep,” Dr. Aouad says. One potential reason behind this is acid reflux, which is when your stomach acid moves up into your throat and causes painful nighttime heartburn. And if you eat food right before bed that makes you gassy, the resulting abdominal pain could drag you out of dreamland, too.

On the flip side, going too long without eating before you sleep can also cause this type of insomnia, Dr. Aouad says. There’s the simple fact that your growling, crampy stomach can wake you up. Hunger could also mess with your blood sugar while you sleep, especially if you have diabetes. Going too long without eating can provoke hypoglycemia, which is when your blood sugar drops too low. This can lead to restless sleep, per the Cleveland Clinic, along with issues like weakness or shaking, dizziness, and confusion. Although hypoglycemia can happen to anyone, it’s much more likely in people with diabetes. If you have the condition, work with your doctor on a plan for keeping your blood sugar stable, including during sleep.

8. You have restless legs syndrome.

Restless legs syndrome, or RLS, may make your lower extremities feel like they are throbbing, itching, aching, pulling, or crawling, among other sensations, according to the National Institute of Neurological Disorders and Stroke (NINDS). If you have RLS, you’ll also feel an uncontrollable urge to move your legs. These symptoms are most common during the evening and night and become more intense during periods of inactivity, like…you guessed it, sleep.

Experts aren’t totally sure what causes RLS, but it seems as though there’s a hereditary factor in the mix, according to the NINDS. Researchers are also investigating how issues with dopamine, a neurotransmitter your muscles need to work correctly, may cause RLS. Sometimes there are other underlying issues bringing about RLS as well, such as iron deficiency.

After diagnosing you with RLS via questions and lab exams, your doctor may prescribe medications to increase your dopamine levels or other drugs, such as muscle relaxants. They may also be able to counsel you on home remedies to soothe your muscles, like warm baths.

To sum it up, there are a bunch of possible reasons you are waking up at night. Some are pretty easy to change on your own, others not so much.

If you think all you need to do to fix this is tweak a habit, like falling asleep with the TV on or chugging a liter of water before bed, start there. If you’ve done everything you can think of and still don’t see a change, it’s worth mentioning your nighttime wakeups to an expert who can help you stay put after you drift off.

 

The Keto Diet for Type 2 Diabetes (How effective is it?)


The conventional approach for Type 2 Diabetes is to manage the condition with medications and diet, based on the American Diabetes Association guidelines, which still includes a lots of high carb foods, along with a low-fat diet and processed vegetable oils. Unfortunately, both science and real-life results show that this protocol just simply does not work. At best, this approach may be better than a junk food diet (but not much better), and have a small shift in blood glucose and other diabetes blood markers if the person has really been abusing their body with junk foods. However, diabetes drugs can often have harmful side effects, and research tells us that the damage to the blood vessels can still occur, even with glucose-lowering diabetes drugs.

While most of general public still keep their bodies fueled on glucose in the form of processed grains, starches, and sugar, (Standard American Diet), others have begun to adopt reduced carb Paleo–and even ketogenic diets that actually reprogram their bodies to the fat burning/fat-fueled machines that our ancestors once had. These kinds of diets are very effective in lowering the amount of glucose circulating in the body, and bringing back insulin sensitivity once again.

What is the difference between a Paleo diet and a Keto diet?

The Paleo diet has been popular the last few years and it is generally a reduced carbohydrate diet compared to the standard Amercian Diet, however “paleo” is only a template for healthy eating, and doesn’t have a specific ratio of carbs like Keto does. However, paleo emphasizes eating foods that our primal ancestors ate: no grains, no dairy, no legumes, no processed foods, and no refined sugar. Paleo does however allow some carbs in the form of sweet potatoes, fruits, starchy vegetables, natural sweeteners like honey, maple syrup and dates. Paleo diets also include grass-fed pastured meats, poultry, eggs, wild caught fish, game and healthy saturated fats.

Is a Paleo diet effective for type 2 diabetes? It is a far cry from the ADA-recommended low-fat/high carb diet and far healthier with its emphasis on fresh veggies, naturally raised proteins, and unprocessed foods, but the Paleo diet can contain variable amounts of carbohydrates and natural sugars, depending on the types of paleo foods you choose to eat. Many versions of Paleo diets include sweet potatoes, or desserts sweetened with dates, honey, molasses, or maple syrup. So, yes, a Paleo diet is a much better choice over the SAD diet, or even the ADA recommended diet, but it’s not always the absolute best choice to lower blood sugar and insulin, depending on the quantity of carbs one chooses to eat on a paleo diet.

On the other hand, the ketogenic diet takes Paleo a step further by restricting carbohydrates to a much larger degree. A keto diet restricts most carbohydrates and all sugar, keeping the resulting glucose in the body consistently low, and forcing your body to burn fats for energy instead of carbs. Keto diets are even more restrictive than Paleo diets as far as carbs go, so in many ways, a keto diet is almost a perfect diet for a diabetic. A keto diet generally allows 20-50 grams of carbohydrates per day. While that is super low compared to the average diet, it can be done, and is easier than you may think.

How a ketogenic diet works for type 2 diabetic

Type 2 diabetes starts when a person is eating large amounts of sugar and carbohydrates. This in turn elevates the body’s serum glucose, creating an increased need for insulin. Over time, the body’s insulin cannot effectively lower the circulating glucose in the body, creating ever higher levels of glucose, insulin, increased body weight, and rising levels of triglycerides. Higher than normal levels of glucose damage blood vessels causing heart disease, kidney disease, blindness and other health issues.

How does a keto diet affect insulin and blood sugar?

When we look at one of the best ways to manage type 2 diabetes, the best and healthiest method is to lower blood sugar by restricting carbohydrates and sugars, in addition to increasing antioxidants and other nutrient-dense foods.

Since a keto diet is a very low carb, low sugar diet, blood sugar stays low, people generally lose weight and the body once again becomes more sensitive to insulin. A keto diet, in comparison to a Paleo diet, allows less carbohydrates and proteins, and adds in more high-quality fats. Because of this drastic dietary transformation, the body quits requiring glucose for energy and instead becomes more efficient in breaking down both dietary fats along with body fat to utilize for energy.

There are many variations on a Paleo diet, but in general a keto diet contains these components:

  • 60-75% of calories from fat (or even more)
  • 15-30% of calories from protein
  • 5-10% of calories from carbohydrates.

The ketogenic diet is not a new dietary fad; it has existed since the 1950’s as a treatment for epilepsy and other health issues. It has recently gained popularity as a way to improve health, increase physical stamina, and lose body fat. A few scientific studies have been conducted on ketogenic diet and diabetes already. Let’s take a look, shall we?

The first study was performed by researchers at Duke University in 2005. Researchers recruited 28 participants with type 2 diabetes who were also overweight. The study lasted 16 weeks. The subjects consumed a low carbohydrate keto diet, aiming for less than 20 grams carbs per day. Diabetics also reduced their medications with medical supervision. There were twenty-one subjects who successfully completed the study. Here’s what they found after only 16 weeks:

  • HbA1c 16% decrease
  • Average 20 lb weight loss
  • Triglyceride levels 42% decrease
  • Ten patients reduced medications, seven stopped medication.

The conclusion of the study was that at keto diet is highly effective at lowering blood glucose, but there should be medical supervision to adjust medications accordingly.

A second study conducted by Stephen Phinney and Jeff Volek, who wrote The Art and Science of Low Carb, showed the positive effects of low carb diet as well. This particular trial shows convincing evidence that a low-carb diet improves blood sugar levels and helps speed weight loss in adults with type 2 diabetes. In almost 60% of participants, diabetes medication was decreased or stopped altogether.

The study, conducted at Indiana University, and published in Journal of Medical Internet Publications, looked at 262 people with type 2 diabetes who were overweight. Participants cut carb intake to 30g a day, while increasing their fats and protein. Patients were also provided nutritional and behavioral counseling, along with digital coaching and medical supervision for medications. Findings after only 10 weeks:

  • HbA1c had a 6.5% decrease
  • BMI decreased by 7%
  • 112 reduced diabetes medications, 21 totally eliminated diabetes medications

Another study of 84 people, looked at the effectiveness of a low-glycemic diet compared to a ketogenic diet, and after 24 weeks looked at key diabetes markers of fasting blood glucose, body mass index (BMI), weight, and Hb A1C. While a low carb, low-glycemic diet is good for controlling diabetes, obviously a keto diet is better.

Low-calorie group

  • Fasting glucose down 16%
  • BMI decreased by 3, average 15lb weight loss
  • .5 reduction in HbA1c

Keto group

  • Fasting glucose down 20%
  • BMI decreased by 4, average 24.5lb weight loss
  • 5 reduction in HbA1c

And this study of 363 overweight or obese participants in the United Arab Emirates looked at the effects of a ketogenic diet on weight loss and diabetes symptoms. 102 of the subjects had type 2 diabetes. One group consumed a low-calorie diet and the other consumed a keto diet. Both groups had nutritional trainer and exercise.

Study subjects were measured on:

  • Body weight
  • BMI
  • Waist circumference
  • Blood glucose
  • HbA1c
  • Cholesterol, LDL, HDL, triglycerides
  • Uric acid, urea, creatinine

After 24 weeks, both groups had improved in all metrics but the keto group had far more significant results. Diabetic medications were decreased to half and some were discontinued for those on the ketogenic diet.

It is important to note for those beginning a ketogenic diet, the drop in glucose can be quick, so it is very important to monitor blood glucose frequently and to have a physician monitor the diabetes medications.

Ketogenic diets are higher in saturated fats, something the American Diabetes Association actually warns diabetics to avoid.  Research, however, shows favorable lipid results on a high fat diet.

In another study, researchers looked at 83 subjects who were divided into three groups of equal calories. One group followed a very low-fat diet, one group followed a diet high in unsaturated fats, and the third group ate a very low carb and high saturated fat diet.

At the end of the 12-week study, all three groups had lost similar amounts of body fat and weight. However, the Low Carb Ketogenic diet group also had the lowest triglyceride levels, higher HDL, and lower glucose and insulin levels.

Very Low-Fat Group:

  • Triglycerides decreased by 4%
  • Insulin levels decreased by 15.1%

High Unsaturated Fat Group:

  • Triglycerides down by 9.6%
  • Insulin levels decreased by 18.7%

Ketogenic Diet Group:

  • Triglycerides decreased by 40%
  • Insulin levels decreased by 33.6%

Key results indicate that ketogenic diets do not increase the risk of heart disease or high cholesterol. Keto diets have shown to significantly decrease harmful lipids including triglycerides and LDL cholesterol, compared to other equal calorie/low fat diets.

Conventional Diabetic Diets vs. Ketogenic Diets  

In spite of all the positive research on ketogenic diets for diabetes, most doctors and dietitians still recommend high carb diets to manage diabetes. A typical medically supervised diet recommended for a type 2 diabetic would include 45-60g carbohydrates at every meal, plus 15-30g of carbs for snacks. Seriously??

Most dietitians and doctors feel that even though the ketogenic diet is effective, most people will not be able to stick to it. And yes, this is somewhat true, although with the emerging popularity of the ketogenic diet, more and more options are available, including recipes, books, blogs, cooking classes, etc. that feature delicious keto meals and snacks. The nature of a keto diet is to keep blood sugar in a low and stable range, and because of this, it is much easier to control appetite and the “munchies”.

Ketogenic diets can be crucial to the successful healthy management of type 2 diabetes. In a recent critical evaluation of literature on carbohydrate restriction and diabetes, a group of 26 leading researchers compiled 12 points of evidence published in the January 2017 Journal of Nutrition, pointing to the use of low carbohydrate diets as the primary dietary treatment of type 2 diabetes. Key points include:

  • Dietary carbohydrate restriction has the greatest effect on decreasing glucose levels.
  • The current epidemic of obesity and diabetes has been caused almost entirely by an increase in carbohydrates.
  • Type 2 diabetics can adhere to a ketogenic diet at least as easily as they can most other diets, and often better.
  • Measured saturated fats in the blood are affected more by dietary carbohydrate intake, than dietary lipid intake.
  • Dietary carbohydrate restriction is the most effective way to reduce serum triglycerides, LDL cholesterol and increasing HDL cholesterol.

Bottom line is that lowering glucose by strictly reducing carbohydrate intake in a ketogenic diet has the most positive effects on diabetes markers, without any of the negative side effects of pharmacological treatments.

All of the available evidence thus far suggests that a keto diet is one of the safest and most effective ways to control or reverse type 2 diabetes. Diabetes patients should always notify their physicians of dietary changes and have medications and blood sugar monitored closely.

Following a strict carbohydrate-restricted, ketogenic diet is key initially, but once your body is adept at fat burning, you may be able to ease up slightly on the daily carbohydrate count. Generally, following a strict keto diet for about 2 months will help your body adapt to burning fat. Rather than stressing out about keeping carbs consistently below 20-30g, it may be easier to give yourself a safe zone to follow. Perhaps one day you eat less, another day you eat more. As long as you generally stick to low carbohydrates, (below 50-60g per day) your body will continue to be fairly efficient in burning fat for energy and keep blood glucose low.

The end result is a healthier body, weight loss and a clear head.  Note that while transitioning to a higher fat ketogenic diet for a type 2 diabetic, you must work closely with your physician to monitor and consistently lower your insulin needs.  With less carbs, you’ll need less insulin.  If you follow keto closely and keep limiting carbs, most Diabetics can get off all medications at some point in time, but it needs to be carefully monitored.

References
https://www.perfectketo.com/keto-diet-vs-paleo-diet-ketosis-better-paleo/

https://www.marksdailyapple.com/keto-and-type-2-diabetes/

Centers for Disease Control and Prevention. National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States, 2014. Atlanta, GA: US Department of Health and Human Services; 2014.
American Diabetes Association. “Nutrition Recommendations and Interventions for Diabetes–2006 A position statement of the American Diabetes Association.”Diabetes care 29.9 (2006): 2140-2157.
Emerging Risk Factors Collaboration. “Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies.” The Lancet 375.9733 (2010): 2215-2222.
O’Gara, Patrick T., et al. “2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.” Journal of the American College of Cardiology 61.4 (2013): e78-e140.
Aguiree, Florencia, et al. “IDF diabetes atlas.” (2013)
“Update 2014”. IDF. International Diabetes Federation. Retrieved 29 November 2014.
Geiss LS, Wang J, Cheng YJ. Thompson TJ, Barker L; Li Y, Albright AL, Gregg EW. Prevalence and incidence trends for diagnosed diabetes among adults aged 20 to 79 years, United States, 1980-2012. JAMA 2014; 312:1218-1226.
Yancy Jr, William S., et al. “A low-carbohydrate, ketogenic diet to treat type 2 diabetes.” Nutr Metab (Lond) 2 (2005): 34.
Westman, Eric C., et al. “The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutr Metab (Lond) 5 (2008): 36.
Hussain, Talib A., et al. “Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes.” Nutrition 28.10 (2012): 1016-1021.
Noakes, Manny, et al. “Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low ‘saturated fat diets on body composition and cardiovascular risk.” Nutrition & metabolism 3.1 (2006): 7

Two New Drug Classes Tied to Better Survival in Type 2 Diabetes


Patients with type 2 diabetes who did not achieve adequate glycemic control with metformin had improved survival during follow-up if they received add-on therapy with a sodium-glucose cotransporter 2 (SGLT-2) inhibitor or a glucagon-like peptide 1 (GLP-1) agonist rather than a dipeptidyl peptidase-4 (DPP-4) inhibitor or control (placebo or no treatment), in a network meta-analysis that indirectly compared these three drug classes.

Rates of heart failure and myocardial infarction (MI) were also lower in patients who received SGLT-2 inhibitors rather than controls.

But GLP-1 agonists were associated with a higher rate of (largely gastrointestinal) adverse events leading to withdrawal from the trials.

These findings, by Sean L Zheng, MB, from the National Heart and Lung Institute at Imperial College, London, UK, and colleagues were published April 17 in JAMA.

“Based on these findings, SGLT-2 inhibition and GLP-1 agonists may be preferred over DPP-4 inhibitors as add-on therapies to metformin,”

In fact, “of the three classes tested, SGLT-2 inhibition may be preferred over the incretin-based therapies based on their association with lower mortality and their favorable adverse event profile,” Zheng and colleagues indicate.

However, they caution that SGLT-2 inhibitors were also associated with increased risk of genital infections, and canagliflozin, but not empagliflozin, was linked with a significant increase in lower-limb amputations. So “our analyses do not rule out the possibility of a clinically meaningful safety signal for SGLT-2 inhibitors and amputation,” they warn.

On the other hand, DPP-4 inhibitors were linked with a greater risk of pancreatitis.

Thus, “careful treatment selection may be necessary to minimize these outcomes in at-risk patients,” Zheng and colleagues advise. Moreover, because the network meta-analysis was an observational study, it cannot determine cause and effect, and the findings would have to be confirmed in further research.

Increasingly Prescribed, But Which Drug Class Is Best?

“The three drug classes assessed here are being increasingly prescribed,” for type 2 diabetes, said Zheng in a statement by Imperial College, “yet until now there have been no clinical trials studying how these drugs compare to each other, and which type of drug could be the best option for patients.”

He and his coauthors searched for studies published up until October 2017 and identified 236 randomized clinical trials in 176,310 patients.

There were 65 trials of SGLT-2 inhibitors, 83 trials of DPP-4 inhibitors, and 65 trials of GLP-1 agonists that compared these agents with a control, and 23 studies that directly compared two drug classes.

Zheng and colleagues aimed to investigate the rate of all-cause mortality (the primary outcome) as well as cardiovascular mortality, heart failure, MI, stroke, adverse events, and hypoglycemia, with use of the three drug classes.

Almost half of the patients came from nine cardiovascular outcome trials: EMPA-REG OUTCOME and CANVAS with SGLT-2 inhibitors; ELIXA, LEADER, SUSTAIN-6, and EXSCEL with GLP-1 agonists; and SAVOR-TIMI 53, EXAMINE, and TECOS with DPP-4 inhibitors.

Overall, during follow-up, patients who received an SGLT-2 inhibitor had a 1% absolute lower rate of death and a 0.8% lower rate of cardiovascular death than patients who received control therapy.

Patients who received a GLP-1 agonist, which are subcutaneously injected, had a “more modest” 0.6% lower risk of death and a 0.5% lower risk of cardiovascular death during follow-up than patients who received control therapy.

However, rates of these two outcomes were similar in patients who received a DPP-4 inhibitor or control therapy.

Expressed another way, patients who received an SGLT-2 inhibitor or a GLP-1 agonist were less likely to die of all causes during follow-up than patients who received control therapy (hazard ratio [HR], 0.80 and 0.88, respectively).

Similarly, patients who received an SGLT-2 inhibitor or a GLP-1 agonist were less likely to die of cardiovascular causes during follow-up than patients who received a DPP-4 inhibitor (HR, 0.78 and 0.0.86, respectively).

The researchers acknowledge a limitation is that they assume there are class effects on mortality. But while, for example, all-cause mortality during follow-up was reduced with GLP-1 agonists liraglutide (in LEADER) and semaglutide (in SUSTAIN-6) it was not with lixisenatide (in ELIXA) or exenatide (in EXSCEL).

Also, the trials may have been too short to detect cardiovascular mortality in patients at low cardiovascular risk, and the meta-analysis did not examine how glycemic control affected mortality.

“Crowded Market” of Second-Line Diabetes Drugs

Separately, an analysis of US sales figures for 2017 shows that sales of GLP-1 agonists rose by 32% in 2017 compared with 2016. Sales of SGLT-2 inhibitors grew by 24% during that time, but sales of DPP-4 inhibitors were flat.

The SGLT-2 inhibitor sales were likely boosted on the one hand by a new US indication for empagliflozin (Jardiance, Lilly/Boehringer Ingelheim), that of improving cardiovascular survival, but were probably diminished by a black-box warning mandated by the Food and Drug Administration for amputations for canagliflozin (Invokana, Janssen).

Meanwhile, Zheng and colleagues say their analysis will help inform patient–physician discussions.

“Our hope is that in the crowded market that is diabetes medications, patients and their doctors have the necessary information to allow them to make informed decisions about long-term treatment strategies,” said Zheng.

The study was supported by a grant from the British Heart Foundation.

Vegan Diet Rapidly Improves Type 2 Diabetes Markers in Adults


In overweight adults with no history of diabetes, a low-fat, plant-based vegan diet can reduce visceral fat and significantly improve both pancreatic beta-cell function and insulin resistance, potentially decreasing the risk of type 2 diabetes, according to researchers.

The 16-week randomized controlled trial in 73 adults showed that participants who ate a diet of vegetables, grains, legumes, and fruits significantly improved their overall metabolic condition, say Hana Kahleova, MD, PhD, of the Physicians Committee for Responsible Medicine in Washington, DC, and colleagues.

“Our study suggests the potential of a low-fat plant-based diet in diabetes prevention, addressing both core pathophysiologic mechanisms — insulin resistance and diminished beta-cell function — at the same time,” they write in their article, published online February 9 in Nutrients.

In a statement by the Physicians Committee for Responsible Medicine, Kahleova said the study “has important implications for diabetes prevention.” An estimated 30 million Americans have type 2 diabetes and it is projected that a third of the population will develop diabetes, she pointed out.

“Fortunately, this study adds to the growing evidence that food really is medicine and that eating a healthful plant-based diet can go a long way in preventing diabetes.”

Vegan vs Normal Diet

Previous studies have shown that the prevalence of diabetes is 46% to 74% lower in people who eat a plant-based diet compared with meat lovers in the general population, according to background information in the article.

 

A vegan diet has also been shown to improve glycemic control in type 2 diabetes better than calorie-restricted, low-carbohydrate diets, the researchers note.

Insulin resistance leading to impaired pancreatic beta-cell function is a key factor in type 2 diabetes, even though current treatment isn’t usually focused on improving beta-cell function, they add.

The study, conducted between October 2016 and June 2017, enrolled eight men and 67 women, age 25 to 75 years, with a body mass index (BMI) of 28 to 40 kg/m2. Participants on the vegan diet were told to avoid animal products and added fats, and they took a daily vitamin B12 supplement (500 μg).

The vegan diet provided 75% of caloric energy from carbohydrates, 15% from protein, and 10% from fats (20–30 grams/day). There was no calorie restriction in the vegan diet. The control group was asked to make no changes to their diet. However, alcohol intake was restricted in both groups: one drink a day for women and two drinks a day for men.

The vegan diet elicited marked increases in meal-stimulated insulin secretion and beta-cell glucose sensitivity, along with decreased fasting insulin resistance and decreased fasting and postprandial plasma glucose concentrations in individuals with no history of diabetes.

Specifically, the homeostasis model assessment – insulin resistance (HOMA-IR) index, used to assess fasting insulin resistance, fell significantly in the intervention group (P < .001), but not in controls (treatment effect −1.0). No significant change in oral glucose insulin sensitivity was observed in either group.

Notably, changes in the HOMA-IR index correlated positively with changes in BMI (r = 0.34; P = .009) and visceral fat volume (r = 0.42; P = .001), and the latter remained significant after adjusting for changes in BMI. Changes in glucose-induced insulin secretion correlated negatively with changes in BMI (r = −0.25; P = .04), but not visceral fat.

In the control group, beta-cell glucose sensitivity did not improve.

As HOMA-IR primarily reflects hepatic insulin resistance, the results “suggest a marked improvement in hepatic, rather than peripheral, insulin sensitivity,” the researchers note. Also, the decrease in insulin resistance was related to loss of visceral fat, independent of changes in BMI, while changes in glucose-induced insulin secretion were related to changes in BMI only.

“In this context, it seems plausible that a low-fat vegan diet in our study decreased hepatic insulin resistance and led to a subsequent improvement in beta-cell function,” the researchers observe.

There was also improvement in plasma lipid concentrations in response to a low-fat vegan diet, which is consistent with previous studies.

Food intake was based on participants’ own dietary records, which may limit the generalizability of the findings, the study authors acknowledge.

Jury Still Out on Benefits of Vegan Diet

As previously reported by Medscape Medical News, the Academy of Nutrition and Dietetics said in its 2016 position statement that plant-based diets are appropriate for people from infancy to old age, and during pregnancy.

For others, however, the jury’s still out on the disease-prevention merits of a vegan diet.

The definition of a plant-based diet can vary widely, the authors of one report point out. Another warns that vegetarian and vegan diets might be associated with nutrient deficiencies that could be harmful during pregnancy.

And recently, a National Institutes of Health study linked a vegetarian diet to higher risk of depression in men.

Monitoring nutritional ketosis with mobile app could reverse Type 2 diabetes


https://speciality.medicaldialogues.in/monitoring-nutritional-ketosis-with-mobile-app-could-reverse-type-2-diabetes/

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