Chart of the Day: Health Spending and Life Expectancy of Selected OECD Countries

Source: The Economist

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The Startling Link Between Sugar and Alzheimer’s

Olga Khazan wrote . . . . . . . . .

In recent years, Alzheimer’s disease has occasionally been referred to as “type 3” diabetes, though that moniker doesn’t make much sense. After all, though they share a problem with insulin, type 1 diabetes is an autoimmune disease, and type 2 diabetes is a chronic disease caused by diet. Instead of another type of diabetes, it’s increasingly looking like Alzheimer’s is another potential side effect of a sugary, Western-style diet.

In some cases, the path from sugar to Alzheimer’s leads through type 2 diabetes, but as a new study and others show, that’s not always the case.

A longitudinal study, published Thursday in the journal Diabetologia, followed 5,189 people over 10 years and found that people with high blood sugar had a faster rate of cognitive decline than those with normal blood sugar—whether or not their blood-sugar level technically made them diabetic. In other words, the higher the blood sugar, the faster the cognitive decline.

“Dementia is one of the most prevalent psychiatric conditions strongly associated with poor quality of later life,” said the lead author, Wuxiang Xie at Imperial College London, via email. “Currently, dementia is not curable, which makes it very important to study risk factors.”

Melissa Schilling, a professor at New York University, performed her own review of studies connecting diabetes to Alzheimer’s in 2016. She sought to reconcile two confusing trends. People who have type 2 diabetes are about twice as likely to get Alzheimer’s, and people who have diabetes and are treated with insulin are also more likely to get Alzheimer’s, suggesting elevated insulin plays a role in Alzheimer’s. In fact, many studies have found that elevated insulin, or “hyperinsulinemia,” significantly increases your risk of Alzheimer’s. On the other hand, people with type 1 diabetes, who don’t make insulin at all, are also thought to have a higher risk of Alzheimer’s. How could these both be true?

Schilling posits this happens because of the insulin-degrading enzyme, a product of insulin that breaks down both insulin and amyloid proteins in the brain—the same proteins that clump up and lead to Alzheimer’s disease. People who don’t have enough insulin, like those whose bodies’ ability to produce insulin has been tapped out by diabetes, aren’t going to make enough of this enzyme to break up those brain clumps. Meanwhile, in people who use insulin to treat their diabetes and end up with a surplus of insulin, most of this enzyme gets used up breaking that insulin down, leaving not enough enzyme to address those amyloid brain clumps.

According to Schilling, this can happen even in people who don’t have diabetes yet—who are in a state known as “prediabetes.” It simply means your blood sugar is higher than normal, and it’s something that affects roughly 86 million Americans.

Schilling is not primarily a medical researcher; she’s just interested in the topic. But Rosebud Roberts, a professor of epidemiology and neurology at the Mayo Clinic, agreed with her interpretation.

In a 2012 study, Roberts broke nearly 1,000 people down into four groups based on how much of their diet came from carbohydrates. The group that ate the most carbs had an 80 percent higher chance of developing mild cognitive impairment—a pit stop on the way to dementia—than those who ate the smallest amount of carbs. People with mild cognitive impairment, or MCI, can dress and feed themselves, but they have trouble with more complex tasks. Intervening in MCI can help prevent dementia.

Rebecca Gottesman, a professor of neurology at Johns Hopkins, cautions that the findings on carbs aren’t as well-established as those on diabetes. “It’s hard to be sure at this stage, what an ‘ideal’ diet would look like,” she said. “There’s a suggestion that a Mediterranean diet, for example, may be good for brain health.”

But she says there are several theories out there to explain the connection between high blood sugar and dementia. Diabetes can also weaken the blood vessels, which increases the likelihood that you’ll have ministrokes in the brain, causing various forms of dementia. A high intake of simple sugars can make cells, including those in the brain, insulin resistant, which could cause the brain cells to die. Meanwhile, eating too much in general can cause obesity. The extra fat in obese people releases cytokines, or inflammatory proteins that can also contribute to cognitive deterioration, Roberts said. In one study by Gottesman, obesity doubled a person’s risk of having elevated amyloid proteins in their brains later in life.

Roberts said that people with type 1 diabetes are mainly only at risk if their insulin is so poorly controlled that they have hypoglycemic episodes. But even people who don’t have any kind of diabetes should watch their sugar intake, she said.

“Just because you don’t have type 2 diabetes doesn’t mean you can eat whatever carbs you want,” she said. “Especially if you’re not active.” What we eat, she added, is “a big factor in maintaining control of our destiny.” Roberts said this new study by Xie is interesting because it also shows an association between prediabetes and cognitive decline.

That’s an important point that often gets forgotten in discussions of Alzheimer’s. It’s such a horrible disease that it can be tempting to dismiss it as inevitable. And, of course, there are genetic and other, non-nutritional factors that contribute to its progression. But, as these and other researchers point out, decisions we make about food are one risk factor we can control. And it’s starting to look like decisions we make while we’re still relatively young can affect our future cognitive health.

“Alzheimer’s is like a slow-burning fire that you don’t see when it starts,” Schilling said. It takes time for clumps to form and for cognition to begin to deteriorate. “By the time you see the signs, it’s way too late to put out the fire.”

Source: The Atlantic

The ‘Bottom’ Blood Pressure Number Matters, Too

Amy Norton wrote . . . . . . . . .

When it comes to blood pressure readings, the “top” number seems to grab all the attention.

But a large, new study confirms that both numbers are, in fact, critical in determining the risk of heart attack and stroke.

Blood pressure measurements are given as a “top” and “bottom” number. The first reflects systolic blood pressure, the amount of pressure in the arteries as the heart contracts. The second reflects diastolic blood pressure, the pressure in the arteries between heart muscle contractions.

For years, systolic blood pressure has been seen as the one that really matters. That’s based on studies — including the famous Framingham Heart Study — showing that high systolic blood pressure is a stronger predictor of heart disease and stroke.

At the same time, though, doctors measure both systolic and diastolic blood pressure, and treatment guidelines are based on both. So just how important is that diastolic number?

“The idea behind this new study was to address the confusion,” said lead researcher Dr. Alexander Flint, an investigator with Kaiser Permanente Northern California’s division of research.

Using medical records from 1.3 million patients, his team confirmed that, yes, high systolic blood pressure was a stronger risk factor for heart attack and stroke. But those risks also climbed in tandem with diastolic pressure; and people with normal systolic readings were still at risk if their diastolic pressure was high.

“There’s been a common belief that systolic blood pressure is the only one that matters,” Flint said. “But diastolic definitely matters.”

He and his colleagues reported the findings in the New England Journal of Medicine.

The definition of high blood pressure has gotten a revamp in recent years. Guidelines issued in 2017 by the American College of Cardiology (ACC) and other heart groups lowered the threshold for diagnosing the condition — from the traditional 140/90 mm Hg to 130/80.

The fact that treatment guidelines include a diastolic pressure threshold implies that it’s important. And indeed it is, said Dr. Karol Watson, a member of the ACC’s prevention section and leadership council.

In fact, she said, doctors once thought that diastolic blood pressure was the more important one — based on research at the time. Then came the studies showing that systolic pressure was generally a better predictor of people’s risk of heart disease and stroke.

In addition, Watson said, high systolic blood pressure is more prevalent, because of natural changes in blood pressure as people age.

“As we get older, systolic blood pressure keeps marching up,” she explained. Diastolic blood pressure, on the other hand, generally peaks when people are in their 40s to 60s — and then it declines.

But it’s clear, Watson said, that while systolic and diastolic blood pressure are different, they both deserve attention.

In the latest study, cardiovascular risks rose with each “unit increase” in systolic pressure above 140, by about 18% on average. Meanwhile, each increase in diastolic blood pressure above 90 was tied to a 6% increase in heart disease and stroke risk.

The researchers saw a similar pattern when they looked at blood pressure increases above the 130/80 threshold. That, Flint said, supports the 2017 guideline shift.

The findings are based on over 1.3 million patients in the Kaiser Permanente health system who had roughly 36.8 million blood pressure readings taken from 2007 through 2016. Over eight years, more than 44,000 patients had a heart attack or stroke.

According to Flint, it’s the largest study of its kind to date.

The bottom line for patients, Watson said, is that they should care about both blood pressure numbers. In her experience, she noted, patients often point to the number that’s in the normal range and say, “But look how good this is.”

Flint agreed, saying that no one should “ignore” the diastolic number. “It’s important not only in blood pressure treatment, but on the side of diagnosis, too,” he said.

Source: HealthDay


Today’s Comic

Blood Pressure Drug Linked with Increased Risk of Bowel Condition

Kate Wighton wrote . . . . . . . . .

A type of blood pressure lowering medication, called a calcium-channel blocker, may be linked with increased risk of bowel condition diverticulosis.

This condition causes small bulges or pouches to appear in the lining of the intestine. Particularly affecting the elderly (as many as 65 per cent of over 85s may be affected), diverticulosis can in some cases can lead to a medical emergency if the pouches become infected or burst.

The new early-stage research finding comes from a team of scientists led by Imperial College London, who investigated the effectiveness and side effects of three common blood pressure medications: ACE-inhibitors, beta-blockers and calcium channel blockers.

High blood pressure affects one in ten adults across the globe, and increases the risk of heart attack and stroke. The most common treatments for high blood pressure are lifestyle changes and medications.

However, despite the three main medications being taken by millions, investigating their potential side effects (as well as studying their effectiveness for treating other diseases), can be difficult and often involves lengthy and expensive clinical trials.

Genetic clues

To overcome this problem, the research team, led by Imperial’s School of Public Health, used genetic analyses to study the effects of the drugs.

By investigating versions of genes that mimic the effects of these drugs, the team were able to study the drugs’ effectiveness – and their potential side effects.

First, the researchers, who published their work in the journal Circulation, identified the proteins targeted by the drugs, and which help lower blood pressure. Next, they analysed genetic data from around 750,000 people and identified the so-called genetic variants that code for these proteins.

The team, who included researchers from LMU Munich, then studied whether these gene variants – which cause increased production of these proteins – were linked to an increased or decreased risk of other diseases.

The good news was that, as expected, these so-called genetic variants (which coded for proteins involved in lowering blood pressure) were linked to lower heart disease and stroke risk.

Increased risk

However after assessing the risk of around 900 different diseases – using data from the UK Biobank study – the team found that the versions of genes related to the effects of a particular type of calcium channel blocker – the non-dihydropyridine class, were linked to an increased the risk of a bowel condition called diverticulosis.

The team compared their findings with further genetic data, and supported the potential link with an increased risk of the bowel condition.

The link now needs further investigation with larger trials, explains Dr Dipender Gill, co-lead author of the research from Imperial’s School of Public Health: “This is the first time that this class of blood pressure drug has been associated with diverticulosis. We’re not sure of the underlying mechanism – although it may relate to effects on the function of intestine muscles, which perform contractions to transport food through the gut.”

Dr Joanna Tzoulaki, senior author from Imperial’s School of Public Health added: “The study of genetic variants that mimic the effect of drugs is evolving as a powerful concept to help prioritise clinical trials and design clinical trials more likely to be successful”.

Dr Gill cautions the findings should not change current prescribing guidelines and that people should not stop taking their medication unless first consulting their doctor.

He added: “These findings should not change clinical practice, but instead should act as a catalyst for further research.”

Source: Imperial College London

At Risk for Alzheimer’s? Exercise Might Help Keep It at Bay

Dennis Thompson wrote . . . . . . . . .

Even if you are at high risk for Alzheimer’s disease, a little more exercise may buy you time, new research suggests.

Folks with elevated levels of a brain protein called beta amyloid tend to be more likely to develop Alzheimer’s disease and experience rapid brain decline later in life, previous research has found.

But apparently they can delay the onset of Alzheimer’s through regular exercise, scientists report.

“People who had elevated levels of amyloid, which is one of the earliest changes you see with Alzheimer’s disease, had slower rates of cognitive decline and brain volume loss over time if they had greater levels of physical activity,” said lead researcher Jennifer Rabin. She is a scientist with the Hurvitz Brain Sciences Program at the Sunnybrook Research Institute in Toronto.

It didn’t take much exercise to enjoy this protection, either.

The data suggests that people who walked 8,300 to 8,900 steps per day significantly delayed the onset of Alzheimer’s, Rabin said.

Previous studies have shown that older people who exercise generally tend to stay sharp longer into old age, but this new research shows physical activity is specifically protective for folks who have these early brain changes related to Alzheimer’s, said Dr. Howard Fillit. He’s executive director and chief science officer at the Alzheimer’s Drug Discovery Foundation.

“This population is different than what’s been studied before because you’re looking at people who are clinically normal but have evidence of Alzheimer’s disease in their brains,” said Fillit, who wasn’t involved with the research.

For this study, Rabin and her colleagues asked 182 participants in the Harvard Aging Brain Study to wear a pedometer for a week, to gauge their usual level of physical activity. Brain scans were used to detect levels of amyloid beta in their brains.

Beta amyloid tends to clump in the brains of Alzheimer’s patients, collecting in sticky plaques between neurons and possibly disrupting brain cell function.

The researchers then tracked the participants over as many as seven years, with annual tests to check the status of their brain function. Repeat scans also were performed to see whether their brains had started to shrink, which is a sign of Alzheimer’s progression.

The study found that people who walked more tended to stay sharper and experience a slower loss of brain volume.

What’s notable is that the brain benefits of exercise were independent of the benefits for heart and blood vessel health, Fillit said.

That means that physical activity is helping the brain in ways beyond preventing micro-strokes that can contribute to dementia, Fillit and Rabin said.

Physical activity might be preserving brain function by reducing inflammation, improving overall flow of blood to the brain, or helping people get better sleep, Rabin said.

Exercise also has been associated with higher levels of BDNF [brain-derived neurotrophic factor], a brain chemical that “is the most powerful neuroprotective growth factor that we know,” Fillit said.

“It doesn’t have to be Tour de France-level training,” Fillit said. “It can just be getting on a treadmill or an elliptical and getting your heart rate up.”

Rabin warned that while physical activity apparently helps mitigate amyloid-related declines in brain function, people with higher levels of beta amyloid are not likely to age as well as those without any amyloid in their brains.

But it’s possible that if those folks combine exercise with heart-healthy habits such as eating right and controlling their blood pressure, they might further reduce their risk of future brain loss, Rabin added.

“If you’re engaging in a host of good lifestyle choices, you maybe could get yourself back to a normal aging trajectory,” Rabin said.

The findings were published online July 16 in the journal JAMA Neurology and presented on the same day at the Alzheimer’s Association International Conference, in Los Angeles.

Source: HealyhDay


Today’s Comic