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Posted by: | Posted on: July 25, 2019

Cholesterol does not cause heart disease

Analysis by Dr. Joseph Mercola Fact Checked July 24, 2019
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2019/07/24/cholesterol-myth-what-really-causes-heart-disease.aspx
cholesterol myth what really causes heart disease

Story at-a-glance

  • A 2018 scientific review presents substantial evidence that high LDL and total cholesterol are not an indication of heart disease risk, and that statin treatment is of doubtful benefit as a form of primary prevention for this reason
  • Three recent reviews that supported the cholesterol hypothesis were found to have misrepresented data and findings of previous studies to support their own conclusions
  • Overall, the analysis found the association between total cholesterol and CVD is weak, absent or inverse in many studies
  • Older people with high LDL do not die prematurely — they actually live the longest, outliving both those with untreated low LDL and those on statin treatment
  • A 2015 meta-analysis of 11 statin drug studies found statin use postponed death by a mere 3.2 days in primary prevention trials and 4.1 days in secondary prevention trials

For the past six decades, the U.S. dietary advice has warned against eating cholesterol-rich foods, claiming dietary cholesterol promotes arterial plaque formation that leads to heart disease. We now have overwhelming evidence to the contrary, yet dogmatic thinking can be persistent, to say the least.

After decades’ worth of research failed to demonstrate a correlation between dietary cholesterol and heart disease, the 2015-2020 Dietary Guidelines for Americans1,2 finally addressed this scientific shortcoming, announcing “cholesterol is not considered a nutrient of concern for overconsumption.”

To this day, the evidence keeps mounting, showing there’s no link between the two. Similarly, the evidence supporting the use of cholesterol-lowering statin drugs to lower your risk of heart disease is slim to none, and is likely little more than the manufactured work of statin makers — at least that’s the implied conclusion of a scientific review3 published in the Expert Review of Clinical Pharmacology in 2018.

Cholesterol myth kept alive by statin advocates?

The 2018 review4 identified significant flaws in three recent studies “published by statin advocates” attempting “to validate the current dogma.” The paper presents substantial evidence that total cholesterol and low-density lipoprotein (LDL) cholesterol levels are not an indication of heart disease risk, and that statin treatment is of “doubtful benefit” as a form of primary prevention for this reason. According to the authors:5

“According to the British-Austrian philosopher Karl Popper, a theory in the empirical sciences can never be proven, but it can be shown to be false. If it cannot be falsified, it is not a scientific hypothesis. In the following, we have followed Popper’s principle to see whether it is possible to falsify the cholesterol hypothesis.

We have also assessed whether the conclusions from three recent reviews by its supporters are based on an accurate and comprehensive review of the research on lipids and cardiovascular disease (CVD) …

Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.”

As reported by Reason.com:6

“A comprehensive new study on cholesterol, based on results from more than a million patients, could help upend decades of government advice about diet, nutrition, health, prevention, and medication …

The study … centers on statins, a class of drugs used to lower levels of LDL-C, the so-called ‘bad’ cholesterol, in the human body. According to the study, statins are pointless for most people …

The study also reports that ‘heart attack patients were shown to have lower than normal cholesterol levels of LDL-C’ and that older people with higher levels of bad cholesterol tend to live longer than those with lower levels.

No evidence cholesterol influences heart disease risk

Indeed, the authors of the Expert Review of Clinical Pharmacology analysis point out that were high total cholesterol in fact a major cause of atherosclerosis, “there should be exposure-response in cholesterol-lowering drug trials.”7 In other words, patients whose total cholesterol is lowered the most should also see the greatest benefit. Alas, that’s not the case.

A review of 16 relevant cholesterol-lowering trials (studies in which exposure-response was actually calculated), showed this kind of exposure-response was not detected in 15 of them. What’s more, the researchers point out that the only study8 showing a positive exposure-response to lowered cholesterol used exercise-only as the treatment.

Patients with high total cholesterol should also be at increased risk of death from CVD, but the researchers found no evidence of this either, not-so-subtly pointing out that this is “an idea supported by fraudulent reviews of the literature.” They provide the following example of how research has been misrepresented:9

“The hypothesis that high TC [total cholesterol] causes CVD was introduced in the 1960s by the authors of the Framingham Heart Study. However, in their 30-year follow-up study published in 1987, the authors reported that ‘For each 1 mg/dl drop in TC per year, there was an eleven percent increase in coronary and total mortality’.

Three years later, the American Heart Association and the U.S. National Heart, Lung and Blood Institute published a joint summary concluding, ‘a one percent reduction in an individual’s TC results in an approximate two percent reduction in CHD risk’. The authors fraudulently referred to the Framingham publication to support this widely quoted false conclusion.”

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Contradictory findings routinely ignored or misrepresented

To determine whether the three reviews under analysis had misrepresented previous findings, they scoured the three papers for quotations from 12 studies reporting results “discordant with the cholesterol hypothesis.” Only one of the three reviews had quoted articles correctly, and even then, only two of the dozen studies were quoted correctly.10

“About half of the contradictory articles were ignored. In the rest, statistically nonsignificant findings in favor of the cholesterol hypothesis were inflated, and unsupportive results were quoted as if they were supportive. Only one of the six randomized cholesterol-lowering trials with a negative outcome was cited and only in one of the reviews.”

The researchers also highlight a large meta-analysis that simply ignored “at least a dozen studies” in which no or inverse association was shown. Overall, the Expert Review of Clinical Pharmacology analysis found that “the association between total cholesterol and CVD is weak, absent or inverse in many studies.”

No link between LDL and heart disease either

The Expert Review of Clinical Pharmacology paper11 also tears apart claims that high LDL causes atherosclerosis and/or CVD. Just as with total cholesterol, if high LDL was in fact responsible for atherosclerosis, then patients with high LDL would be diagnosed with atherosclerosis more frequently, yet they’re not, and those with the highest levels would have the greatest severity of atherosclerosis, yet they don’t.

The researchers cite studies showing “no association” between LDL and coronary calcification or degree of atherosclerosis. Ditto for LDL and CVD. In fact, a study looking at nearly 140,000 patients with acute myocardial infarction found them to have lower than normal LDL at the time of admission.

Even more telling, another study, which had originally reported similar findings, still went ahead and lowered the patients’ LDL even more. At follow-up three years later, they discovered that patients with an LDL level below 105 mg/dl (2 mmol/L) had double the mortality rate of those with higher LDL.12

Interestingly, the authors suggest this inverse relationship may be due to low LDL increasing your risk for infectious diseases and cancer, both of which are common killers.

They also review evidence showing older people with high LDL do not die prematurely — they actually live the longest, outliving both those with untreated low LDL and those on statin treatment. One such study13,14 — a meta-analysis of 19 studies — found 92% of individuals with high cholesterol lived longer.

Benefits of statin treatment are overblown

Lastly, the Expert Review of Clinical Pharmacology paper analyzes statin claims, showing how studies exaggerate benefits through a variety of different tactics. Again, in some cases, by simply excluding unsuccessful trials.

“Furthermore, the most important outcome — an increase of life expectancy — has never been mentioned in any cholesterol-lowering trial, but as calculated recently by Kristensen et al.,15 statin treatment does not prolong lifespan by more than an average of a few days,” the authors state.16

Indeed, the study they’re referring to, published in BMJ Open in 2015, which looked at 11 studies with a follow-up between two and 6.1 years, found “Death was postponed between -5 and 19 days in primary prevention trials and between -10 and 27 days in secondary prevention trials.” The median postponement of death in primary prevention trials was 3.2 days, and in secondary prevention trials 4.1 days!

Considering the well-documented health risks associated with statins, this is a mind-bending finding that really should upend the dogma. And yet, the dogma remains, and may even strengthen in coming days.

JAMA editorial calls for end to ‘fake news’ about statins

The cholesterol myth has been a boon to the pharmaceutical industry, as cholesterol-lowering statins — often prescribed as a primary prevention against heart attack and stroke — have become one of the most frequently used drugs on the market. In 2012-2013, 27.8% of American adults over the age of 40 reported using a statin, up from 17.9% a decade earlier.17,18 But that was six years ago, I suspect over a third of adults over the age of 40 are now using statins.

In addition to the BMJ Open study cited above, an evidence report19 by the U.S. Preventive Services Task Force, published November 2016 in JAMA, found 250 people need to take a statin for one to six years to prevent a single death from any cause; 233 had to take a statin for two to six years to prevent a single cardiovascular death specifically. To prevent a single cardiovascular event in people younger than 70, 94 individuals would have to take a statin.

As noted in a 2015 report,20 “statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease.” The paper points out that by using a statistical tool known as relative risk reduction, the trivial benefits of statins appear greatly amplified.

Scientific findings such as these are the core reason why statins are given negative press. However, we may soon see a reversal in the news cycle, with negative statin articles being tagged as “fake news.”

According to a June 2019 editorial21 in JAMA Cardiology, written by cardiologist Ann Marie Navar,22 statins are the victim of “fear-based medical information,” just like vaccines, and this is what’s driving patient nonadherence. Cardiovascular Business reported:23

“We know that what people read influences their actions, Navar said, and indeed, one 2016 study in the European Heart Journal found that on a population level, statin discontinuation increased after negative news stories about statins surfaced in those communities.

In another study, more than one in three heart patients said they declined a statin prescription solely for fears of adverse effects. ‘Measles outbreaks are highly visible: a rash appears, public health agencies respond, headlines are made and the medical community responds vocally,’ Navar wrote.

‘In contrast, when a patient who has refused a statin because of concerns stoked by false information has an MI, the result is less visible. Nevertheless, cardiologists and primary care physicians observe the smoldering outbreak of statin refusal daily.’”

Cardiovascular Business summarizes Navar’s suggestions for how doctors can fight back against false information about statins and build adherence, such as handing out yearlong prescriptions with automatic refills.24

When I first wrote about the censorship of anti-vaccine material occurring on every single online platform, I warned that this censorship would not stop at vaccines. And here we’re already seeing the call for censoring anti-statin information by glibly labeling it all “fake news.”

Chances are, the censoring of anti-statin information is already underway. A quick Google search for “statin side effects” garnered pages worth of links talking about minor risks, the benefits of statins, comparison articles, looking at two different brands — in other words, mostly positive news.

The scientific fact is, aside from being a “waste of time” and not doing anything to reduce mortality, statins also come with a long list of potential side effects and clinical challenges, including:

An increased risk for diabetes
Decreased heart function25
Nutrient depletions — Including CoQ10 and vitamin K2, both of which are important for cardiovascular and heart health
Impaired fertility — Importantly, statins are a Category X medication,26 meaning they cause serious birth defects,27 so they should never be used by a pregnant woman or women planning a pregnancy
Increased risk of cancer — Long-term statin use (10 years or longer) more than doubles women’s risk of two major types of breast cancer: invasive ductal carcinoma and invasive lobular carcinoma28
Nerve damage — Research has shown statin treatment lasting longer than two years causes “definite damage to peripheral nerves”29

How to assess your heart disease risk

cholesterol levels

As a general rule, cholesterol-lowering drugs are not required or prudent for the majority of people — especially if both high cholesterol and longevity run in your family. Remember, the evidence overwhelmingly suggests your overall cholesterol level has little to nothing to do with your risk for heart disease.For more information about cholesterol and what the different levels mean, take a look at the infographic above. You can also learn more about the benefits of cholesterol, and why you don’t want your level to be too low, in “Cholesterol Plays Key Role in Cell Signaling.” As for evaluating your heart disease risk, the following tests will provide you with a more accurate picture of your risk:

HDL/Cholesterol ratio — HDL percentage is a very potent heart disease risk factor. Just divide your HDL level by your total cholesterol. That percentage should ideally be above 24%.
Triglyceride/HDL ratio — You can also do the same thing with your triglycerides and HDL ratio. That percentage should be below 2.
NMR LipoProfile Large LDL particles do not appear to be harmful. Only small dense LDL particles can potentially be a problem, as they can squeeze through the lining of your arteries. If they oxidize, they can cause damage and inflammation.

Some groups, such as the National Lipid Association, are now starting to shift the focus toward LDL particle number instead of total and LDL cholesterol to better assess your heart disease risk. Once you know your particle size numbers, you and your doctor can develop a more customized program to help manage your risk.

Your fasting insulin level — Heart disease is primarily rooted in insulin resistance,30 which is the result of a high-sugar diet. Sugar, not cholesterol or saturated fat, is the primary driver. Clinical trials have shown high fructose corn syrup can trigger risk factors for cardiovascular disease within as little as two weeks.31

Any meal or snack high in carbohydrates like fructose and refined grains generates a rapid rise in blood glucose and then insulin to compensate for the rise in blood sugar.

The insulin released from eating too many carbs promotes fat accumulation and makes it more difficult for your body to shed excess weight. Excess fat, particularly around your belly, is one of the major contributors to heart disease.

Your fasting blood sugar level — Research has shown people with a fasting blood sugar level of 100 to 125 mg/dl have a nearly 300% increased higher risk of coronary heart disease than people with a level below 79 mg/dl.32,33
Your iron level — Iron can be a very potent oxidative stress, so if you have excess iron levels you can damage your blood vessels and increase your risk of heart disease. Ideally, you should monitor your ferritin levels and make sure they are not much above 80 ng/ml.

The simplest way to lower them if they are elevated is to donate your blood. If that is not possible you can have a therapeutic phlebotomy and that will effectively eliminate the excess iron from your body.

Posted by: | Posted on: July 11, 2019

Anticholinergic drugs increase your risk for dementia

Analysis by Dr. Joseph Mercola Fact Checked
anticholinergic medication and dementia

Story at-a-glance

  • While dementia and Alzheimer’s disease (the most advanced, severe and lethal form of dementia) are primarily diet- and lifestyle-driven, certain medications can also ramp up your risk
  • One of the riskiest classes of drugs in this regard are anticholinergic drugs, prescribed for a wide variety of conditions, including depression, incontinence, insomnia, allergies and epilepsy
  • Recent research assessing effects of 56 anticholinergics found statistically significant associations between dementia and anticholinergic antidepressants, antiparkinson drugs, antipsychotic drugs, bladder antimuscarinics and antiepileptic drugs
  • In the highest exposure group (excess of 1,095 standardized daily doses over the past one to 11 years before diagnosis), the odds ratio for dementia was between 44% and 54%, with an average of 49%; anticholinergic antipsychotics raise risk by 70%
  • A 2009 scientific review found all but two of 27 studies found an association between the anticholinergic activity of medications and either delirium, cognitive impairment or dementia

While dementia and Alzheimer’s disease (the most advanced, severe and lethal form of dementia) are primarily diet- and lifestyle-driven, certain medications can also ramp up your risk.

One of the riskiest classes of drugs in this regard are anticholinergic drugs, prescribed for such widely varying conditions such as depression, incontinence, insomnia, allergies and epilepsy.1 You can find a long list of anticholinergic drugs and the different conditions they’re used for on seniorlist.com.2

Anticholinergic drugs block acetylcholine, a neurotransmitter that performs important functions in your peripheral and central nervous systems, both as an activator and an inhibitor.3

For example, it triggers muscle contractions and pain responses, and is involved in the regulation of your endocrine system and REM sleep cycle. Of all the known neurotransmitters, acetylcholine is the most abundant.4

As reported by CNN,5 a recent observational study6 looking at anticholinergics and dementia risk “suggests that the link is strongest for … antidepressants such as paroxetine or amitriptyline, bladder antimuscarinics such as oxybutynin or tolterodine, antipsychotics such as chlorpromazine or olanzapine and antiepileptic drugs such as oxcarbazepine or carbamazepine.”

Study highlights risks of anticholinergic drugs

The research,7,8 published online in JAMA Internal Medicine, June 24, 2019, assessed data from 58,769 patients over the age of 55 diagnosed with dementia and 225,574 matched controls.

In all, the outcomes for 56 different anticholinergic drugs were assessed by looking at exposure to “standardized daily doses” of the drugs prescribed over the previous one to 11 years before the patient received a diagnosis of dementia.

After controlling for confounding variables that might influence the results, the researchers concluded “there were statistically significant associations of dementia risk with exposure to anticholinergic antidepressants, antiparkinson drugs, antipsychotic drugs, bladder antimuscarinics and antiepileptic drugs.”

Compared to those who did not use anticholinergic drugs, those in the lowest exposure group (taking between just one and 90 standardized doses over the previous one to 11 years), the adjusted odds ratio for dementia was, on average, 6%.

In the highest exposure group (excess of 1,095 standardized daily doses over the past one to 11 years before diagnosis), the odds ratio for dementia was between 44% and 54%, with an average of 49%. Even between the different types of anticholinergics there were significant variations in risk. Among those with the highest exposure:

  • Anticholinergic antidepressants had an average adjusted odds ratio for dementia of 29%
  • Antiepileptic drugs had an average adjusted odds ratio of 39%
  • Antiparkinson drugs 52%
  • Bladder antimuscarinic drugs (prescribed for overactive bladder9) 65%
  • Antipsychotics 70%

Middle-aged individuals urged to minimize exposure

The strongest associations were seen in those diagnosed with dementia before the age of 80. The adjusted odds ratio for those in the highest exposure group who were diagnosed with dementia after the age of 80 was 35%, while the odds for those diagnosed before the age of 80 was a whopping 81%.10

No significant gender differences were found. Overall, vascular dementia was more common than Alzheimer’s disease, with odds for vascular dementia in the highest exposure group being 68% compared to 37% for Alzheimer’s.11 As noted by the authors:
“Exposure to several types of strong anticholinergic drugs is associated with an increased risk of dementia. These findings highlight the importance of reducing exposure to anticholinergic drugs in middle-aged and older people.”
“No significant increases in risk” for dementia were found for anticholinergic antihistamines, muscle relaxants, antispasmodics (prescribed for gastrointestinal problems), antiarrhythmics and antimuscarinic bronchodilators.12

 


Avoiding anticholinergics may improve cognition, says JAMA study

While the authors of the featured JAMA study point out it cannot prove causality, it’s not the first study to find this link. There are quite a few of them in the medical literature, which you can find by searching PubMed.gov, the free online library of medicine run by the U.S. National Institutes of Health.13

Among them you’ll find the 2009 paper,14 “The Cognitive Impact of Anticholinergics: A Clinical Review,” which analyzed the results of 27 studies in which “anticholinergic activity was systematically measured and correlated with standard measurements of cognitive performance.”

According to the authors, “All but two studies found an association between the anticholinergic activity of medications and either delirium, cognitive impairment or dementia,” which led to the conclusion that:
“Medications with anticholinergic activity negatively affect the cognitive performance of older adults. Recognizing the anticholinergic activity of certain medications may represent a potential tool to improve cognition.”

Some anticholinergics clearly worse than others

A case-control study15 published in 2018 in the BMJ — which like the featured JAMA study looked at the effects of various classes of anticholinergics — also found that antidepressant, urological and antiparkinson drugs posed the greatest risk. As noted by the authors:16
“It is well known that anticholinergics affect cognition, and guidelines suggest they are to be avoided among frail older people. Use of anticholinergic drugs among people with dementia is recognized as inappropriate by both the Beers and the Screening Tool of Older Persons’ potentially inappropriate Prescriptions (STOPP) criteria.
Over the past decade, prolonged exposure to anticholinergic drugs has been linked to long term cognitive decline or dementia incidence among community living cohorts and nursing home residents.”
Here, the researchers included 40,770 patients newly diagnosed with dementia, and compared their outcomes with their use of anticholinergic drugs four to 20 years before their diagnosis.

Each patient was compared to as many as seven matched controls who did not have dementia. The median age at diagnosis was 83 and the median drug exposure period was 7.1 years.17 The study had three stated objectives:18

  1. Assessing the effect of chronic anticholinergic drug use on dementia incidence
  2. Exploring whether observed effects are restricted to any particular drug class. Drugs were divided into three groups based on the “anticholinergic cognitive burden (ACB) scale,”19 where a score of 3 means the drug has “definite anticholinergic activity” and is known to significantly raise the risk of cognitive impairment
  3. Testing how the risk might vary based on the amount of exposure to any given drug class and the timing of use

The primary analysis found “a positive and significant association” between anticholinergics and dementia, regardless of their ACB score. Those with an ACB score of 1 and 2 had an odds ratio of 10% and drugs with an ACB score of 3 had an odds ratio of 11%.

The primary difference between the ACB classes were the dose-response effect. Drugs with an ACB score of 2 or 3 had a clear dose-dependent response, whereas drugs with a score of 1 did not.20 As for objective 2, the researchers found:
“When analyzed by class, there was a significant association between dementia incidence and any prescription of antidepressant, antiparkinson, or urological drugs with an ACB score of 3, but no association with antispasmodic, antipsychotic, antihistamine, or other drugs with an ACB score of 3.
Prescriptions for drugs with an ACB score of 2 were relatively rare, and so results are imprecise in this group, but there is some evidence for an association between dementia incidence and prescription of antiparkinson drugs.
We found positive associations for antidepressant drugs with an ACB score of 1 with an increased risk of dementia, but not with any other drugs with an ACB score of 1.”
Lastly, the timing of the drug exposure was assessed, looking at three different sets of time intervals: four to 10 years, 10 to 15 years, and 15 to 20 years of use before dementia diagnosis. For drugs with an ACB score of 3, the risk was “consistent” across all three exposure periods, although the strongest association was seen for ACB 3-class drugs used for 15 to 20 years before diagnosis. For this group, the odds ratio for dementia was between 10% and 24%, with an average of 17%.

Antidepressants and urological drugs with an ACB score of 3 “remained consistently significantly associated with dementia incidence,” with antidepressants having an average odds ratio of 19% and urological drugs 27%.21 For drugs with ACB scores of 1 and 2, the risks became more apparent closer to the date of diagnosis. As noted by the authors:
“[F]or antidepressants with an ACB score of 1, the association with dementia increased for prescriptions given in periods closer to a diagnosis of dementia. Similarly, the negative association between gastrointestinal drugs and dementia was not seen for exposures 15-20 years before the index date.”

Behavioral changes can be an early sign of dementia

As you can see, even within a single class of drugs, in this case, drugs broadly classified as anticholinergics, you find all sorts of factors that can increase or decrease their risks to any given individual.

Overall, however, anticholinergics as a group are risky, and the risk of dementia increases the longer you’re on them. Even if the drug in question has a low ACB score, if you’re on it for decades, the risk of dementia creeps up. It would be wise for everyone to be on the lookout for early signs of dementia, but especially so if you’re on an anticholinergic drug.

Now, dementia is not a disease in itself; it’s a term used to describe a number of different brain illnesses that may affect your memory, thinking, behavior and ability to perform everyday activities. Many people associate dementia with memory loss — and this is a red flag — however, not all memory problems are due to dementia or Alzheimer’s.

As noted by the Alzheimer’s Association,22 some causes of dementia-like symptoms (including memory loss), such as those related to thyroid problems and vitamin deficiencies, are reversible with proper treatment.

Before memory and thinking problems become obvious, people with dementia will often display changes in mood and behavior. A person may, for instance, stop doing something they’ve always loved to do, be it cooking a certain dish for your birthday or watching the evening news.

Apathy is another common sign, although some people may display more blatant changes like suddenly becoming sexually promiscuous or developing the habit of snatching food from other people’s plates.23,24

At the 2016 Alzheimer’s Association International Conference, a group of Alzheimer’s experts presented a 34-question checklist25 of signs of mild behavioral impairment (MBI), which they believe might help identify patients at high risk for Alzheimer’s.

Those with sudden mood or behavioral changes that persist tend to develop dementia at a faster rate.26,27 The MBI checklist was published in the Journal of Alzheimer’s Disease in 2017.28 You can find a copy of the questionnaire here.

Is it age-related forgetfulness or something more serious?

Aside from that, the Alzheimer’s Association has also compiled a list29 of early signs and symptoms of Alzheimer’s, along with suggestions for how to determine whether you’re dealing with typical age-related changes or something more serious:

Signs of Alzheimer’s/dementia Typical age-related changes
Poor judgment and decision-making Making a bad decision once in a while
Inability to manage a budget Missing a monthly payment
Losing track of the date or the season Forgetting which day it is and remembering it later
Difficulty having a conversation Sometimes forgetting which word to use
Misplacing things and being unable to retrace steps to find them Losing things from time to time

As mentioned at the outset, Alzheimer’s is primarily diet- and lifestyle driven. In fact, it shares many risk factors with heart disease, including insulin resistance and diabetes. For a list of dietary strategies and general lifestyle guidelines that can help prevent Alzheimer’s, see “Link Between Sugar and Alzheimer’s Strengthens.”

To learn more about Alzheimer’s and the tests that can help diagnose it early, see my interview with Dr. Dale Bredesen, author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.”

Sources and References