Wellness

[Trinity11]

@cherry...it was 1921 regarding the discovery of insulin.

[cherry]

I thought that was wrong @Trinity11. I recall them talking about the discovery of insulin  on Downton Abbey.. It must be a typo  or something

snip

CHARLES H. BEST

Charles H. Best was born in 1899 in Washington County, Maine and moved to Toronto in 1915 to study at the University of Toronto.  As a fourth year student in the Honours Physiology and Biochemistry course, Best was introduced to Frederick Grant Banting by his professor and mentor, John J.R. Macleod, along with fellow student, Clark Noble.  The two were recommended as assistants to Banting to conduct research on the pancreas and its connection to diabetes.  Best and Noble tossed a coin to decide who would obtain the coveted research position, resulting in Best being the auspicious victor. 

SOURCE: http://livinghistory.med.utoronto.ca/people/charles-h-best

The research that Banting and Best did in their small, decrepit laboratory in the physiology department led to one of the most groundbreaking discoveries in medical history for the University of Toronto.  The duo found that isolating this pancreatic hormone, insulin, and purifying it became a highly effective treatment for type 1 diabetes.  In 1923, these efforts were recognized and awarded with a Nobel Prize in Physiology or Medicine to Frederic G. Banting and John J.R. Macleod.  While Banting and Macleod were the official recipients of the award, Banting shared his prize money with Best and the two went down in history as the co-discoverers of insulin.

Following the discovery of insulin, Charles Best headed the Physiology Department beginning in 1927 and, at age thirty-one, became one of the youngest departmental chairs in the history of the faculty.  During his years as head of the department, Best co-authored a textbook in 1937 with Norman B. Taylor entitled, The Physiological Basis of Medical Practice, which is said to have put the medical school in Toronto on the international map with respect to the teaching of physiology.  Upon Banting’s death in 1941, Best became the head of the Banting and Best Department of Medical Research (BBDMR) in addition to his departmental chair responsibilities.  He relinquished his positions in 1965 due to a depressive illness and in 1978, Best became critically ill after hearing of the death of his older son, Sandy, and died shortly thereafter.

[cherry]

Pre-exercise Breakfast May Allow for Increased Glycemic Management

Sep 29, 2018

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New study shows that consuming pre-exercise breakfast lowers insulin levels at subsequent meals.

Diet and exercise are arguably the most heavily discussed topics when it comes to diabetes, and, more specifically, patients with type 2 diabetes. Exercise is known to play an important role in the removal of glucose from the bloodstream into skeletal muscle where it can be utilized as energy, and has thus been encouraged in many patients with diabetes looking to enhance their glycemic control.

In a new study published in the American Journal of Physiology-Endocrinology and Metabolism, investigators sought to take on a new angle in regards to diet and exercise associated with blood sugar levels. Investigators of the study postulated that the majority of studies done on glycemic response in relation to exercise are not representative of daily living in the mainstream population. The majority of exams and studies done, they attest, are performed when patients are in the fasted state rather than in the postprandial state, which is how most people in developed countries spend their time. The aim of this study, therefore, was to examine postprandial plasma glucose levels after three different states: breakfast-rest, breakfast-exercise, and overnight-fasted exercise.

A randomized cross-over design was used to evaluate 12 men who self-reported to regularly participate in at least 30 minutes of exercise, three days per week. Participants with a history of metabolic disease or any other health condition that may have put the participant at risk were excluded from the study results.

Study participants refrained from taxing physical activity and consuming both alcohol and caffeine for 24 hours prior to onset of the study. Fasting began 12 hours before the testing period where only water was consumed. In the breakfast-exercise and breakfast-rest state, participants consumed an oatmeal and milk breakfast (431 kcal), whereas in the overnight-fasted exercise state, no food was consumed. In the breakfast-exercise and overnight-fasted exercise state, participants engaged in 60 minutes of cycling while in the breakfast-rest state, no exercise was done during this period.

Expired gas samples and blood samples were collected at baseline and throughout the tests, as well as a 2-hour oral glucose tolerance test (2-h OGTT) with 73g of glucose. Muscle samples were also collected both at baseline and post-exercise or rest.

Statistical analysis was performed using ANOVA tests to determine the differences between baseline and summary measurements.

Results were shown through both plasma glucose disappearance rate and plasma glucose appearance rate and compared between states. Investigators found that consuming breakfast prior to exercise led to an increased rate of glucose disappearance during and after exercise compared to the extended overnight fasting state. They also examined plasma insulin concentrations and found that insulin levels were lower in participants who consumed breakfast prior to exercise than those who fasted.

These results allowed investigators to conclude that consuming a breakfast prior to exercise does in fact increase the plasma glucose expulsion during subsequent meals consumed after exercise, despite lower plasma levels of insulin. They conferred that consuming breakfast both improved glucose tolerance as well as insulin sensitivity after subsequent meals, and that this may be the first study to determine these results.

Glycemic management can be labeled as the most important factor when it comes to preventing complications associated with diabetes. The results from this trial are not only compelling to scientists in the diabetes community, they could become a framework for a new set of guidelines when it comes to diet and exercise in patients with diabetes.

Practice Pearls:

• Rates of plasma glucose disposal into skeletal muscle post-exercise are higher in patients who consume breakfast prior to exercise than those who fasted.
• Pre-exercise consumption of breakfast lowers insulin levels at subsequent meals following exercise.
• Tests performed in the fasted state cannot be inferred to the fed state, as this study showed that glycemic response in each state varies significantly.
• Further studies are needed employing larger population size along with both sexes to solidify claims made in this study.

Reference:

Edinburgh, R. M., Hengist, A., Smith, H. A., Travers, R. L., Koumanov, F., Betts, J. A., Gonzalez, J. T. (2018). Pre-Exercise Breakfast Ingestion versus Extended Overnight Fasting Increases Postprandial Glucose Flux after Exercise in Healthy Men. American Journal of Physiology-Endocrinology and Metabolism. doi:10.1152/ajpendo.00163.2018

Clarke Powell, Pharm.D. Candidate 2019, LECOM School of Pharmacy

[cherry]

Having type 1 diabetes is not associated with an increased risk of developing a hearing impairment, research has found.

Scientists compared 1,150 people with type 1 diabetes with 283 of their partners who did not have the condition - the results indicated no overall difference in hearing ability in both groups.

However, the findings also revealed that people with type 1 diabetes who had higher HbA1c readings for longer periods of time did have a greater risk of developing a hearing impairment.

The study was carried out following previous research which indicated an association between diabetes and hearing impairment, but only in studies with small numbers.

This project was the largest of its kind, with the research team recruiting participants from the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) study, which has been following the lives of people with type 1 diabetes for more than 30 years.

People who took part in the study had their ears tested at pitches associated with speech as well as at very high ranges.

A total of 20% of participants who had type 1 diabetes complained of speech-level hearing impairment compared to 19% of their partners.

When it came to hearing sound at very high pitches, 52% of those with type 1 diabetes and 48% of their spouses recorded impaired hearing.

The similar results led the researchers to conclude: "We found no significant difference in the prevalence of hearing impairment between the group with type 1 diabetes and the spousal control group. Among those with type 1 diabetes, higher mean HbA1c over time was associated with hearing impairment."

Commenting on the research, JDRF said: "These findings are good news for people living with type 1 diabetes and their quality of life. However, in their paper, the researchers noted that the relatively young age of the participants (on average 56 years old) may be why they generally found low levels of hearing impairment, as hearing loss tends to develop at an older age."

The research was limited to exploring the hearing of married people, who tend to be healthier, so the conclusions may not be representative of everyone with type 1 diabetes.

[cherry]

Beta cells are the body’s insulin factories. Found in the pancreas, they respond to blood glucose levels, churning out more insulin to signal muscle cells to absorb the glucose from the bloodstream.

In people with diabetes, beta cells don’t produce sufficient insulin. In people with type 2 diabetes, that’s because the beta cells fail over time. In people with type 1, the body’s immune system malfunctions and attacks the beta cells.

In some people with diabetes, beta cell failure is the result of faulty genes. Over the past decade, researchers have identified a handful of spots where a tiny mistake in a patient’s genetic code can interfere with the body’s ability to sense or produce insulin. The result is what doctors call monogenic diabetes.

Such single-gene mutations are responsible for more diabetes cases than generally recognized. Dieter Egli, PhD, a stem cell biologist at the Naomi Berrie Diabetes Center at Columbia University Medical Center in New York, says 1 to 5 percent of people with diabetes has some variety of monogenic diabetes, adding up to millions of people around the world. “It’s not such a rare phenomenon,” he says.

For decades, replacing failing beta cells has been the holy grail of treatment for all types of diabetes. Researchers have tried everything from pancreas transplants to beta cells surgically implanted in patients. But the replacement beta cells come at a high cost: Because they’re foreign cells, the body tends to reject them. Controlling the immune reaction requires powerful immunosuppressant drugs or encapsulation of the transplanted beta cells.

Because monogenic diabetes is the result of a single genetic flaw, or mutation, new technologies offer the promise of a cure for people with forms of monogenic diabetes. And the innovative treatment could perhaps lead to therapies for some type 2 patients. With the help of a grant from the American Diabetes Association, Egli and his team of scientists are working with monogenic diabetes patients—specifically, people with neonatal diabetes, whose inability to produce insulin appears at birth or shortly thereafter—to test a different approach. They start by creating stem cells, which are cells that can be shaped into specific tissues, from beta cells to nerves.

Then Egli uses a cutting-edge technique with the unwieldy name of CRISPR-Cas9 to fix the genetic mistakes that prevent beta cells from working. Over the past year, the research has yielded promising results. “We’ve been able to correct the mutation in stem cells and make insulin-producing beta cells,”  Egli says. “We showed, in principle, that it can be done.”

The next step would be to implant the corrected, lab-grown beta cells back into the patient. Because they’re grown from the patient’s own cells, they should be accepted by the body without the need for immunosuppressant drugs. And because they’re functional beta cells, they should respond to blood glucose levels and produce insulin the way normal beta cells do.

The science behind gene editing is still new, however, and not yet approved by the Food and Drug Administration (FDA) for testing in humans. To see if the beta cells worked, Egli took the corrected human beta cells and put them in lab animals bred to have beta cells that don’t work. “By grafting the beta cells into mice, we can protect beta cell–deficient mice from diabetes,” says Egli. “These are human cells that cure a mouse. It’s really something different.”

Egli says if the corrected beta cells can be safely implanted into a person with monogenic diabetes or even forms of type 2 that have a strong genetic cause, it would amount to a diabetes cure. “The beta cells will become part of the person,” he says.

Lots of work remains to be done before the gene editing techniques are ready to use in people. Some researchers worry that the techniques used to edit mutations could cause unintended, “off-target” effects elsewhere. “The mouse is a great model, but some answers we will only learn if we try them in humans,” Egli says.

Even if Egli and others in the field can prove that personalized gene therapy is safe, it will be a long time before it’s cost-effective compared with test strips, glucose meters, and insulin injections. While patients would no longer have to pay for insulin and other diabetes management supplies, personalized stem cell therapy could cost tens of thousands of dollars per patient, or more.

Egli is optimistic—particularly for people with no ability to produce insulin, such as the neonatal diabetes patients he is working with.

For now at least, so-called personalized gene therapy is easiest to apply in cases where problems producing insulin are the result of pinpoint errors that can be readily reversed, as with monogenic diabetes. However, Egli says he can imagine a future where more complex cases can also benefit from gene therapy: “Many people with type 2 may have mutations that are not well-characterized,” he says. Future research might identify cases where gene therapy could reduce type 2 risk. Likewise, stem cell–derived beta cells may one day be used to treat people with type 1 diabetes.

[cherry]

Experts Say High Cholesterol Does Not Cause Heart Disease

Photo by iStockPhoto

By Maria Muccioli Ph.D.

September 18th, 2018

For decades, medical practitioners have been advising their patients to keep total and LDL-cholesterol levels within a certain range to protect against cardiovascular disease (CVD). Now, a new expert literature review is challenging the idea that serum cholesterol levels are an independent risk factor for CVD.

Major Findings

The international team of sixteen experts identified considerable flaws in three recent reviews on the subject, and presented substantial evidence showing that total and LDL-cholesterol levels are not indicative of CVD risk. Specifically, the authors noted that:

• Total cholesterol levels are generally NOT associated with atherosclerosis severity
• Total cholesterol levels are generally NOT predictive of CVD risk
• In many studies, LDL-cholesterol levels are NOT associated with atherosclerosis
• A large study showed that individuals who experienced a heart attack generally had lower LDL-cholesterol levels
• Among adults over 60 years old, those with higher LDL-cholesterol levels generally live longer
• Among those with familial hypercholesterolemia (FH), few individuals die prematurely
• There is no difference in LDL-cholesterol levels among individuals with FH who have CVD and those who don’t

Photo by Adobe Stock Photos

Also, the experts expressed criticism of the wide-spread use of statin (cholesterol-lowering) drugs. Specifically, they explained that:

• Clinical trials of statin drugs did not show a true exposure-response relationship
• Statin benefits have been exaggerated, and even questioned
• Statin treatment can result in considerable side effects

Implications for People with Diabetes

These findings are especially relevant to people with diabetes who are considered at higher risk to develop CVD. Recent recommendations have even suggested statin therapy for all individuals with diabetes starting at age 40. Meanwhile, in addition to well-established side effects, at least one study has demonstrated that statin therapy appears to increase fasting blood glucose levels, especially in individuals with diabetes.

Photo by Adobe Stock Photos

Conflict of Interest

Of the seventeen authors, one declared a patent on a “homocysteine-lowering protocol,” while seven others authored or edited books that criticize the current cholesterol dogma. No other “relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript” were declared by the review authors. The peer reviewers of the manuscript did not declare any conflict of interest.

Conclusions

“For half a century, a high level of total cholesterol (TC) or low-density-lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated, and that statin treatment, in particular when used as primary prevention, is of doubtful benefit,” the authors stated in the review abstract.

Strikingly, the expert reviewers noted that, “in our analysis of three major reviews, that claim the cholesterol hypothesis is indisputable and that statin treatment is an effective and safe way to lower the risk of CVD, we have found that their statements are invalid, compromised by misleading statistics, by exclusion of unsuccessful trials, by minimizing the side effects of cholesterol lowering, and by ignoring contradictory observations from independent investigators.”

In summary, an international panel of experts agree that the current dogma suggesting that high LDL-cholesterol levels can cause CVD is highly misleading, while the benefits of cholesterol-lowering statin drugs have been over-stated.

[cherry]

High cholesterol ‘does not cause heart disease’

Cholesterol does not cause heart disease in the elderly and trying to reduce it with drugs like statins is a waste of time, an international group of experts has claimed.

A review of research involving nearly 70,000 people found there was no link between what has traditionally been considered “bad” cholesterol and the premature deaths of over 60-year-olds from cardiovascular disease.

Published in the BMJ Open journal, the new study found that 92 percent of people with a high cholesterol level lived longer.

The authors have called for a re-evaluation of the guidelines for the prevention of cardiovascular disease and atherosclerosis, a hardening and narrowing of the arteries, because “the benefits from statin treatment have been exaggerated”.

The results have prompted immediate scepticism from other academics, however, who questioned the paper’s balance.

High cholesterol is commonly caused by an unhealthy diet, and eating high levels of saturated fat in particular, as well as smoking.

It is carried in the blood attached to proteins called lipoproteins and has been traditionally linked to cardiovascular diseases such as coronary heart disease, stroke, peripheral arterial disease and aortic disease.

Co-author of the study Dr Malcolm Kendrick, an intermediate care GP, acknowledged the findings would cause controversy but defended them as “robust” and “thoroughly reviewed”.

“What we found in our detailed systematic review was that older people with high LDL (low-density lipoprotein) levels, the so-called “bad” cholesterol, lived longer and had less heart disease.”

Vascular and endovascular surgery expert Professor Sherif Sultan from the University of Ireland, who also worked on the study, said cholesterol is one of the “most vital” molecules in the body and prevents infection, cancer, muscle pain and other conditions in elderly people.

“Lowering cholesterol with medications for primary cardiovascular prevention in those aged over 60 is a total waste of time and resources, whereas altering your lifestyle is the single most important way to achieve a good quality of life,” he said.

Lead author Dr Uffe Ravnskov, a former associate professor of renal medicine at Lund University in Sweden, said there was “no reason” to lower high-LDL-cholesterol.

But Professor Colin Baigent, an epidemiologist at Oxford University, said the new study had “serious weaknesses and, as a consequence, has reached completely the wrong conclusion”.

Another sceptic, consultant cardiologist Dr Tim Chico, said he would be more convinced by randomised study where some patients have their cholesterol lowered using a drug, such as a stain, while others receive a placebo.

He said: “There have been several studies that tested whether higher cholesterol increases the risk of heart disease by lowering cholesterol in elderly patients and observing whether this reduces their risk of heart disease.

“These have shown that lowering cholesterol using a drug does reduce the risk of heart disease in the elderly, and I find this more compelling than the data in the current study.”

The British Heart Foundation also questioned the new research, pointing out that the link between high LDL cholesterol levels and death in the elderly is harder to detect because, as people get older, more factors determine overall health.

“There is nothing in the current paper to support the author’s suggestions that the studies they reviewed cast doubt on the idea that LDL Cholesterol is a major cause of heart disease or that guidelines on LDL reduction in the elderly need re-valuating,” a spokesman said.

[cherry]

Lipid‐Lowering Medication Decreases Risk of Diabetic Retinopathy in Type 2 Diabetes

Published on October 1, 2018

By : Suvarna Sheth

Using lipid-lowering medication with fibrates, including fenofibrate and statins reduces not only the incidence of diabetic retinopathy in patients with Type 2 diabetes but also the need for treatment in those who already have the condition, a Japanese study finds.

Researchers at Osaka University Graduate School of Medicine in Japan analyzed data on almost 85,000 patients with Type 2 diabetes for their study.

Their results show that the incidence of diabetic retinopathy was reduced by about 23% with the use of lipid-lowering medication, and fibrates and statins were similarly effective.

They also found the need for diabetic retinopathy treatment among patients with Type 2 diabetes who already had the complication was reduced by 35% with lipid-lowering medication, and the need for laser photocoagulation and vitrectomy was reduced by 35% and 52%, respectively.

According to a Medscape article, the results follow data from the ACCORD study, which showed that combining fenofibrate with a statin reduced the rate of progression of diabetic retinopathy, and an analysis of the FIELD study indicated that fenofibrate reduced the need for laser treatment of diabetic retinopathy.

The article also notes that the use of fenofibrate to slow the progression of existing diabetic retinopathy in people with Type 2 diabetes is to date only approved in Australia.

Study Design

Researchers gathered information from the health claims database of the Japan Medical Data Center, Tokyo, on adults with Type 2 diabetes or unspecified diabetes and a prescription for a glucose-lowering medication from 2005 to 2017.

They divided the claims into a baseline period of 2005 to 2013 and a follow-up period of 2014 to 2017.

The participants were divided into two groups: one that did not have diabetic retinopathy during the baseline period to determine the incidence of diabetic retinopathy during the follow-up period.69,070 individuals were reported in this group.

The second group consisted of individuals diagnosed with diabetic retinopathy during the baseline period. This group was recruited to determine the incidence of diabetic macular edema and the use of diabetic retinopathy-related treatments during the follow-up period.

Of the participants, 20.9% were prescribed standard statins, such as simvastatin and pravastatin, and 79.1% “strong” statins, which included atorvastatin and rosuvastatin. In addition, 54.4% were prescribed bezafibrate and 45.5% fenofibrate.

During the 3-year follow-up, 7110 individuals developed diabetic retinopathy. And lipid-lowering medication was associated with a significantly reduced incidence of diabetic retinopathy, with 7.4% of patients treated with the drugs developing the complication versus 11.4% of patients not treated.

Kawasaki says the study suggests that lipid-lowering medication is beneficial for both the incidence and progression of diabetic retinopathy, however, he notes the study was observational and limited to health claims data without clinical quantitative variables such as glucose level or severity of retinopathy.

Kawasaki says more research is needed on this promising topic.

Full research findings can be read here.

The study was supported by research grants provided by Novartis Pharma and Pfizer, Japan.

Sources:

1. “Statins, Fibrates Lower Diabetic Retinopathy Risks in Diabetes,” Davenport, Liam. September 28, 2018. Retrieved from: https://www.medscape.com/viewarticle/902675#vp_3

2. “Lipid‐lowering medication is associated with a decreased risk of diabetic retinopathy and the need for treatment in patients with type 2 diabetes: A real‐world observational analysis of a health claims database,” Ryo Kawasaki Ph.D., Tsuneo Konta Ph.D., Kohji Nishida Ph.D. First published: 22

[cherry]

There is controversy about statins ,and like everything else you should talk to your Dr before you make any decisions  about stopping them

I don't take them, I can't ,but I do not have heart disease, and my arteries are clear. What works for me, might not for you. My cholesterol is borderline high ,and always has been. So was my mothers, but her heart was fine. There is no history of heart disease in my family

I posted these articles to show ,you must be careful about who you believe, and your Dr should always be your first source of advice , they know you best

[tansy]

@Trinity11, FYI I did encounter a defective sensor last night.  I had problems assembling it, decided to inject it anyway, but the reader wouldn’t recognize it.  I called Abbott and will receive a replacement but am required to return the sensor, applicator and box.  It also takes 12 hours to charge.