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Showing posts sorted by relevance for query Alzheimer’s disease. Sort by date Show all posts
Showing posts sorted by relevance for query Alzheimer’s disease. Sort by date Show all posts

Monday, 28 August 2017

The Ketogenic Diet Improves Cognitive Function

The first trial using the ketogenic diet (KD) in patients with Alzheimer’s disease was presented at the 2017 Alzheimer’s Association International Conference. It was presented in session of the Conference that was dedicated to the potential benefits of ketones called: Brain Ketone Metabolism, Ketogenic Interventions and Alzheimer’s disease.

As discussed in another blog post, it is know that in Alzheimer’s disease, the brain loses its ability to uptake and use glucose. This decreased glucose utilization results in decrease energy (ATP) production, causing an energy deficit in the brain. It is believed that this energy deficit then increases the risk of neuronal dysfunction and cognitive decline. Specifically, it has been shown that patients with early Alzheimer’s disease have 20-30% less glucose uptake and utilization in certain areas of the brains compared to cognitively normal older adults. Research by Dr. Cunnane, has shown that the uptake and utilization of ketones is the same in brains of patients with Alzheimer’s disease compared to the brains of cognitively normal older adults. (Cunnane, 2016)

This research by Dr Cunnane shows that the even the areas of the Alzheimer’s brains that had decreased uptake of glucose had normal uptake of ketones. The implication of this is that the neurons themselves are not dead just not able to use glucose. The hope is that ketones can help improve cognition by improving this brain energy deficit. This was the basis of the KU Alzheimer’s Disease Ketogenic Diet study. The objection of the study was to see if by changing the fuel source from glucose to ketones thru the KD, would result in improvement of cognitive symptoms in patients with Alzheimer’s disease.

The KU Alzheimer’s Disease Ketogenic Diet Feasibility and Retention Trial


The KU Alzheimer’s Disease Ketogenic Diet Feasibility and Retention Trial, involved 15 patients with a diagnosis of mild Alzheimer’s disease. The 15 patients were placed on the KD and an additional triglyceride supplement for 3 months. The degree of ketosis was measured thru urine and plasma ketone levels. Cognitive function tests were assessed at baseline, at the end of the 3 months, and then a month later after back on a regular diet.

Out of the 15 patients, 5 were able to unable to achieve ketosis and dropped out of the study. The 10 that were able to get into ketosis and remain on the diet for 3 months, showed an improvement in cognitive function of 4.1 points on the Alzheimer’s Disease Assessment Scale-Cog (ADAS Cog) score. After returning back to a standard diet, the scores then dropped back down to their baselines values.

The author of the study, Dr. Swerdlow, was noted to say: “As far as Alzheimer’s studies go, a 4 point improvement in the ADAS Cog score is fairly robust.” “It suggests a meaningful improvement in cognition.” “It is greater than that seen in the cholinesterase inhibitors studies.” (Hughes, 2017)

Data from this study supports the need for further studies of KD in Alzheimer’s disease. The intervention was well tolerated without serious adverse event. The main limitation of the study was adhering to the KD. (Swerdlow, 2017) Dr. Swerdlow noted that the KD is not an easy diet to be on, and potentially an easier way to get ketones to the brain may be with supplements, which does not require such a strict low carbohydrate diet.


Graham

Tuesday, 28 July 2015

High Blood Sugar May Boost Alzheimer's Risk

High blood sugar associated with prediabetes may increase the risk for Alzheimer's disease, a new study suggests.

Researchers found that insulin resistance -- higher-than-normal levels of blood sugar that often precede type 2 diabetes -- was related to poorer performance on memory tests taken by late-middle-age adults.

"The findings are interesting because people with diabetes are at increased risk for developing Alzheimer's disease, but we are only now learning why they may be at increased risk," said lead researcher Barbara Bendlin, an assistant professor of medicine at the University of Wisconsin-Madison.

The study results suggest that insulin resistance could increase the risk for Alzheimer's disease by altering the way the brain uses sugar (glucose), which is its primary fuel, she said.

However, "by altering insulin resistance in midlife, it may be possible to reduce future risk of Alzheimer's disease," Bendlin said. Medications and a healthy lifestyle are possible ways to do that, she said.

According to the American Diabetes Association, 29.1 million Americans have diabetes, and more than half of adults older than 64 have prediabetes. Poor diet, obesity and sedentary lifestyles are associated with insulin resistance, Bendlin noted.

"Healthier lifestyles may contribute to healthier brain aging by reducing insulin resistance," Bendlin said.

One expert cautioned that having prediabetes, or insulin resistance, doesn't mean you're doomed to develop Alzheimer's, the most common form of dementia.

This study shows that insulin resistance may make mental functioning worse and may be linked to reduced use of insulin in areas of the brain associated with Alzheimer's disease, but this does not mean that insulin resistance leads to Alzheimer's, said Dr. Luca Giliberto, an investigator at the Litwin-Zucker Research Center for the Study of Alzheimer's Disease at the Feinstein Institute for Medical Research in Manhasset, N.Y.

"We do not know what causes Alzheimer's disease," said Giliberto, who was not involved in the study. "We don't know if lowering blood sugar will prevent Alzheimer's."

For the study, Bendlin's team gave memory tests to 150 adults with no mental impairments, at average age of 61. The researchers also measured insulin resistance and had the participants undergo a PET brain scan.

More than two-thirds of the participants had a parent who suffered from Alzheimer's, about 40 percent had a gene mutation associated with increased Alzheimer's risk and roughly 5 percent had type 2 diabetes, according to the study.

The researchers found insulin resistance was associated with poorer processing of sugar throughout the brain. Worse performance in immediate memory was linked to lower sugar metabolism in the left medial temporal lobe, the authors said.

The report was published July 27 online in JAMA Neurology.

Dr. Sam Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York City, said it appears there may be a difference "between the dementia related to full-blown diabetes, which seems to be primarily dementia caused by hardening of the arteries in the brain, and the mental impact of insulin resistance, which some investigators believe is associated with Alzheimer's."

In the brain, insulin helps transmit messages between cells, he noted.

"We have long thought of Alzheimer's as a disease of defective brain signaling," said Gandy, who had no role in the study. "Conceivably, there is also a disease of defective insulin signaling, which this paper would support."

If that's true, Gandy added, "then efforts at sensitizing the brain to insulin, using drugs such as pioglitazone [Actos, a diabetes drug], would make sense and might well lead to slowing of degeneration."

Giliberto recommended healthy living as the best way to keep blood sugar under control and perhaps protect mental health.

"Increasing our health by reducing fats, reducing sugar, improving insulin resistance may reduce the risk of other factors, such as diabetes, on the susceptibility to Alzheimer's disease and mental decline," Giliberto said. 

http://www.everydayhealth.com/

Graham

Saturday, 13 April 2019

Case Study Supports Keto As Treatment For Alzheimer’s disease


This article written by Bret Scher, MD FACC and taken from Diet Doctor site:

"As we have written before, the rates of Alzheimer’s disease are predicted to sky rocket in the near future with a potential devastating toll on families and medical costs. As a result, pharmaceutical companies are investing billions of dollars to search for a cure. Unfortunately, the result has been one spectacular failure after the next.

Yet a small case series, published books and various anecdotal reports suggest a ketogenic diet may be the most promising tool we have for treating Alzheimer’s disease. A new publication in the journal Alzheimer’s & Dementia adds to the growing body of evidence.

Alzheimer’s & Dementia: APOE ε4, the door to insulin-resistant dyslipidemia and brain fog? A case study

The authors of this case report hypothesize that those with ApoE4 variants (a genetic variant that is known to increase the risk for Alzheimer’s disease) have reduced ability to clear the beta-amyloid plaque from the brain, and they may have reduced ability to transport lipids among the neurons, thus increasing the formation of reactive oxygen species. This combination places them at increased risk for developing Alzheimer’s disease, especially if they have any element of insulin resistance or type 2 diabetes.

With the mounting evidence that Alzheimer’s disease may result from insulin resistance in the brain and inability to properly utilize glucose as fuel, suddenly it makes sense why a ketogenic diet may be the ideal treatment.

The recently published case report highlights the beneficial effects of a keto diet on one individual with type 2 diabetes, Alzheimer’s disease, and the Apo E4 variant. After only 10 weeks on a clinically prescribed ketogenic diet, the subject improved his cognitive assessment score from mild dementia to normal, his HbA1c normalized from 7.8% to 5.5%, and his other metabolic biomarkers likewise improved.

This does not prove that a ketogenic diet will be the magical cure for Alzheimer’s disease, but it certainly is more encouraging than all of the pharmaceutical drug failures. Instead of targeting the amyloid plaques, as many drugs do, we are better off focusing on the metabolic changes that occur in the brain, helping the brain decrease insulin resistance, or even providing the brain with ketones as an alternative fuel source. The mounting anecdotal evidence gives us hope that the cure for a seemingly complex and devastating condition may be as simple as what we choose to eat. Stay tuned to our blog, as we will continue to report on the science as we learn more about the intersection between Alzheimer’s disease and ketogenic diets."

Many thanks for reading - if you would like to read other articles related to Alzheimer’s disease - please click on the link
here

All the best Jan

Tuesday, 11 August 2015

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet.

Us diabetics hear so much about blindness, limb amputation and kidney failure, it is not surprising we fear these complications the most. As all know here these complications can be avoided, and in some cases reversed if treated quickly and earlier enough. In my time I have seen family and friends die from all sorts of causes, the worst I have seen is Alzheimer's disease, it is a truly horrible way to check out. This is an interesting read and once again our old friend low carb high fat may be the answer.

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet.

"Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease.

A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with alzheimer's disease, and may also be due in large part to this same underlying cause. 
  
Recent population studies have confirmed a correlation between low blood serum cholesterol and both dementia and Parkinson's disease. A study published in 2007 compared three elderly population groups: subjects with dementia, subjects with depression, and controls. They found that those with dementia and depression had significantly lower serum cholesterol levels than the controls.Another study looking at Parkinson's disease among the elderly showed that those with the lowest LDL had 3.5 times the risk of Parkinson's disease compared to those with the highest serum LDL levels.

"Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease." 

My bold.

Link to the full paper here and well worth your time reading I reckon.

Eddie

Friday, 17 March 2017

Type 3 Diabetes: The Alarming Link Between Alzheimer’s and Diet

Michael Joseph at Nutrition Advance writes:

"If you haven’t heard of it, type 3 diabetes is what many specialists are now calling Alzheimer’s disease.
The name covers the belief that Alzheimer’s results from insulin resistance of the brain.

Alzheimer’s is a cruel, degenerative condition that devastates millions of lives around the world.

And unfortunately, it’s only increasing in prevalence; as of 2016, 1 in 9 people over the age of 65 have Alzheimer’s.

Surprisingly, the number of individuals aged 65 and over with the condition is expected to triple by the year 2050.

This article takes a look at the metabolic theory of type 3 diabetes, and how we might be able to prevent (or potentially halt) the condition.

What is Type 3 Diabetes?
Type 3 diabetes—or Alzheimer’s disease—is a chronic condition in which brain neurons slowly degenerate and die.
As a result, we see progressive memory loss and rapid declines in cognitive ability.

I’ve personally seen the terrible effects of Alzheimer’s. As a young boy, I remember seeing my great grandfather hospitalized with late-stage Alzheimer’s.
And then from the start of my late teenage years, I saw my granddad—a strong, well-built man—slowly succumb to the disease.

Sadly, the condition can hit anyone.

Someone being physically fit or having an intelligent mind is not relevant; the disease doesn’t discriminate, and it takes no prisoners.

A Cruel Condition
Experiencing a slow deterioration, patients eventually lose the ability to interact with their environment, communicate, and even remember their family.
Ultimately, Alzheimer’s disease is fatal, and patients usually die from a resulting complication such as pneumonia.
Worse still, it’s not only the patient that suffers.
Alzheimer’s caregivers often have to spend all their time and money to look after their family member, and it’s a very emotionally and physically demanding job.

Key Point: Alzheimer’s Disease is a devastating condition that is rapidly increasing in prevalence. It slowly and progressively robs people of their ability to think, move, communicate, and live everyday life.

Why is Alzheimer’s ‘Type 3 Diabetes’?
There are three types of diabetes:
Type 1 diabetes occurs when the pancreas cannot produce insulin.

When the body cannot produce enough insulin and becomes resistant to insulin’s effects, a type 2 diabetes diagnosis follows.

Type 3 diabetes is now being used to describe Alzheimer’s, due to the brain insulin resistance link. Generally speaking, diagnosis usually occurs in those over the age of 65, but the disease can develop over decades.

More and more researchers are saying that type 3 diabetes is one of the “diseases of civilization.”

This term refers to the fact that how we live our life can significantly impact our health.
For instance, our diet, exercise plan, and sleep can either dramatically increase or reduce our risk of diseases such as:
Alzheimer’s
Cancer (some types)
Cardiovascular Disease
Diabetes
Rheumatoid Arthritis
These ‘diseases of civilization’ are part of the metabolic syndrome, and glucose and insulin dysregulation profoundly influence all of them.

The Harms of the Modern Western Diet

For the most part, these problems stemming from glucose and insulin issues relate to the food we eat.
And unfortunately, the modern Western—perhaps global—diet revolves around industrially processed food.
In fact, a study analyzing consumer purchases shows that 77% of all grocery purchases are either moderately (16%) or highly (61%) processed.
These foodstuffs contain significant amounts of sugar and refined carbohydrates, leading to large spikes in blood sugar and insulin levels.
Over time, this can lead to worsening insulin resistance and eventually, metabolic disease.

Key Point: What causes Alzheimer’s disease? While there may not be a single answer, the modern Western diet likely plays a huge role.

The Alarming Link Between Type 3 Diabetes and Diet
there is a strong connection between type 3 diabetes and the food we eat.
But what, precisely, does the science say?

Can We Reverse Type 3 Diabetes With Diet?"



Please go and read more, find out more, all with relevant links here

All the best Jan

Monday, 10 March 2014

Alzheimer's: new test is 'major step forward'

"US researchers say tests on markers in blood allowed them to forecast with 90pc accuracy whether a person would develop Alzheimer's within three years"
"A blood test for Alzheimer’s capable of predicting whether a person will develop dementia has been developed in a breakthrough hailed by campaigners.
The test could ultimately lead to successful treatment that would halt or even prevent the disease, scientists said.
The research found that biomarkers in the blood could be used to forecast whether a person would develop Alzheimer’s disease within three years with a 90 per cent level of accuracy.
Charities on Sunday said the findings from the American trial were encouraging and could signify an important advance in dementia treatment.
However, they also warned of ethical dilemmas ahead and said patients must be given a choice about whether they wanted to receive potentially devastating news about their future."
Full story here.
The $64,000 questions, would you take the test ? would you want to know ? Can you do anything to ward off Alzheimer’s ? Maybe you can !
"Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease.

A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with alzheimer's disease, and may also be due in large part to this same underlying cause.
  
Recent population studies have confirmed a correlation between low blood serum cholesterol and both dementia and Parkinson's disease. A study published in 2007 compared three elderly population groups: subjects with dementia, subjects with depression, and controls. They found that those with dementia and depression had significantly lower serum cholesterol levels than the controls. Another study looking at Parkinson's disease among the elderly showed that those with the lowest LDL had 3.5 times the risk of Parkinson's disease compared to those with the highest serum LDL levels.

"Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease."


Information source and more can be found here.

Eddie

Tuesday, 11 February 2014

Diabetes and Alzheimer's disease

I posted this up a few years ago, more and more we are hearing about diabetes and Alzheimer's disease. Well worth a read if you missed it the first time around.

Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease.

A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with alzheimer's disease, and may also be due in large part to this same underlying cause.
  
Recent population studies have confirmed a correlation between low blood serum cholesterol and both dementia and Parkinson's disease. A study published in 2007 compared three elderly population groups: subjects with dementia, subjects with depression, and controls. They found that those with dementia and depression had significantly lower serum cholesterol levels than the controls. Another study looking at Parkinson's disease among the elderly showed that those with the lowest LDL had 3.5 times the risk of Parkinson's disease compared to those with the highest serum LDL levels.

"Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease."


Information source and more can be found here.

Eddie

Friday, 30 June 2017

Alzheimer's and the benefits of low carb higher fat diet.

Yesterday Phil a reader and commenter here, sent us a link regarding some news regarding diet and Alzheimer's. The full article is here.

"The Mediterranean diet is associated with a variety of health benefits, including a lower incidence of dementia. Now, researchers have identified a specific ingredient that protects against cognitive decline: extra-virgin olive oil. In a new study, the researchers show that consumption of extra-virgin olive oil protects memory and learning ability and reduces the formation of amyloid-beta plaques and neurofibrillary tangles in the brain -- classic markers of Alzheimer's disease."


At this time there is no cure for Alzheimer's, once diagnosed it progresses at various speeds in different people. Jan's mother passed away around three years after diagnosis, a friend of our's dear wife, was in a care home for eighteen years before she succumbed. If we cannot cure Alzheimer's can we prevent this horrible disease. Can a healthier diet help? is there a healthy diet? that could give us a better chance to stay mentally fit for longer. It appears there is, some extracts from a very interesting paper.

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet.

"Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. 

Recent population studies have confirmed a correlation between low blood serum cholesterol and both dementia and Parkinson's disease. A study published in 2007 compared three elderly population groups: subjects with dementia, subjects with depression, and controls. They found that those with dementia and depression had significantly lower serum cholesterol levels than the controls.Another study looking at Parkinson's disease among the elderly showed that those with the lowest LDL had 3.5 times the risk of Parkinson's disease compared to those with the highest serum LDL levels.

Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease."



As you would expect, our little team believes, a whole fresh food lifestyle, is the only way to go, to give a person a fighting chance to stay healthy. Unfortunately there are no guarantees in this life. The good news is, in the nine years we have been using and writing about, the low carb higher healthy natural fats lifestyle, we have never ever encountered or learned of any downsides whatsoever. The upsides have been many.

Eddie

Tuesday, 22 July 2014

Stephanie Seneff: Why Low-Fat Diets And Statins May Cause Alzheimer's

MONDAY, JULY 21, 2014

APOE-4: THE CLUE TO WHY LOW-FAT DIET AND STATINS MAY CAUSE ALZHEIMER'S

ABSTRACT

Alzheimer's is a devastating disease whose incidence is clearly on the rise in America. Fortunately, a significant number of research dollars are currently being spent to try to understand what causes Alzheimer's. ApoE-4, a particular allele of the apolipoprotein apoE, is a known risk factor. Since apoE plays a critical role in the transport of cholesterol and fats to the brain, it can be hypothesized that insufficient fat and cholesterol in the brain play a critical role in the disease process. In a remarkable recent study, it was found that Alzheimer's patients have only 1/6 of the concentration of free fatty acids in the cerebrospinal fluid compared to individuals without Alzheimer's. In parallel, it is becoming very clear that cholesterol is pervasive in the brain, and that it plays a critical role both in nerve transport in the synapse and in maintaining the health of the myelin sheath coating nerve fibers. An extremely high-fat (ketogenic) diet has been found to improve cognitive ability in Alzheimer's patients. These and other observations described below lead me to conclude that both a low-fat diet and statin drug treatment increase susceptibility to Alzheimer's.

1. INTRODUCTION


Alzheimer's is a devastating disease that takes away the mind bit by bit over a period of decades. It begins as odd memory gaps but then steadily erodes your life to the point where around-the-clock care is the only option. With severe Alzheimer's, you can easily wander off and get lost, and may not even recognize your own daughter. Alzheimer's was a little known disease before 1960, but today it threatens to completely derail the health system in the United States.

Currently, over 5 million people in America have Alzheimer's. On average, a person over 65 with Alzheimer's costs three times as much for health care as one without Alzheimer's. More alarmingly, the incidence of Alzheimer's is on the rise. Dr. Murray Waldman has studied epidemiological data comparing Alzheimer's with femur fractures, looking back over the last fifty years [52]. Alarmingly, he has found that, while the incidence of femur fractures (another condition which typically increases with age) has gone up only at a linear rate, the increase in the incidence of Alzheimer's has gone up exponentially, between 1960 and 2010 Alzheimer's Epidemic [15]. Just between 2000 and 2006, US Alzheimer's deaths rose by 47%, while, by comparison, deaths from heart disease, breast cancer, prostate cancer, and stroke combined decreased by 11%. This increase goes far beyond people living longer: for people 85 and older, the percentage who died from Alzheimer's rose by 30% between 2000 and 2005 [2]. Finally, it's likely these are under-estimates, as many people suffering with Alzheimer's ultimately die of something else. You likely have a close friend or relative who is suffering from Alzheimer's.

Something in our current lifestyle is increasing the likelihood that we will succumb to Alzheimer's. My belief is that two major contributors are our current obsession with low-fat diet, combined with the ever expanding use of statin drugs. I have argued elsewhere that low-fat diet may be a major factor in the alarming increase in autism and adhd in children. I have also argued that the obesity epidemic and the associated metabolic syndrome can be traced to excessive low-fat diet. Statins are likely contributing to an increase in many serious health issues besides Alzheimer's, such as sepsis, heart failure, fetal damage, and cancer, as I have argued here. I believe the trends will only get worse in the future, unless we substantially alter our current view of "healthy living."

The ideas developed in this essay are the result of extensive on-line research I conducted to try to understand the process by which Alzheimer's develops. Fortunately, a great deal of research money is currently being spent on Alzheimer's, but a clearly articulated cause is still elusive. However, many exciting leads are fresh off the press, and the puzzle pieces are beginning to assemble themselves into a coherent story. Researchers are only recently discovering that both fat and cholesterol are severly deficient in the Alzheimer's brain. It turns out that fat and cholesterol are both vital nutrients in the brain. The brain contains only 2% of the body's mass, but 25% of the total cholesterol. Cholesterol is essential both in transmitting nerve signals and in fighting off infections.

A crucial piece of the puzzle is a genetic marker that predisposes people to Alzheimer's, termed "apoE-4." ApoE plays a central role in the transport of fats and cholesterol. There are currently five known distinct variants of apoE (properly termed "alleles"), with the ones labelled "2", "3" and "4" being the most prevalent. ApoE-2 has been shown to afford some protection against Alzheimer's; apoE-3 is the most common "default" allele, and apoE-4, present in 13-15% of the population, is the allele that is associated with increased risk to Alzheimer's. A person with apoE-4 allele inherited from both their mother and their father has up to a twenty-fold increased likelihood of developing Alzheimer's disease. However, only about 5% of the people with Alzheimer's actually have the apoE-4 allele, so clearly there is something else going on for the rest of them. Nonetheless, understanding apoE's many roles in the body was a key step leading to my proposed low fat/statin theory.


Read more here:  http://www.allouteffort.com/

Graham

Monday, 27 February 2023

'Fructose may bear some responsibility for Alzheimer’s'

 "Study suggests fructose could drive Alzheimer's disease

An ancient human foraging instinct, fuelled by fructose production in the brain, may hold clues to the development and possible treatment of Alzheimer's disease (AD), according to researchers at the University of Colorado Anschutz Medical Campus.

The study, published recently in The American Journal of Clinical Nutrition, offers a new way of looking at a fatal disease characterized by abnormal accumulations of proteins in the brain that slowly erode memory and cognition.

"We make the case that Alzheimer's disease is driven by diet," said the study's lead author Richard Johnson, MD, professor at the University of Colorado School of Medicine specializing in renal disease and hypertension. The study co-authors include Maria Nagel, MD, research professor of neurology at the CU School of Medicine.

Johnson and his team suggest that AD is a harmful adaptation of an evolutionary survival pathway used in animals and our distant ancestors during times of scarcity.

"A basic tenet of life is to assure enough food, water and oxygen for survival," the study said. "Much attention has focused on the acute survival responses to hypoxia and starvation. However, nature has developed a clever way to protect animals before the crisis actually occurs."

When threatened with the possibility of starvation, early humans developed a survival response which sent them foraging for food. Yet foraging is only effective if metabolism is inhibited in various parts of the brain. Foraging requires focus, rapid assessment, impulsivity, exploratory behavior and risk taking. It is enhanced by blocking whatever gets in the way, like recent memories and attention to time. Fructose, a kind of sugar, helps damp down these centers, allowing more focus on food gathering.

In fact, the researchers found the entire foraging response was set in motion by the metabolism of fructose whether it was eaten or produced in the body. Metabolizing fructose and its byproduct, intracellular uric acid, was critical to the survival of both humans and animals.

The researchers noted that fructose reduces blood flow to the brain's cerebral cortex involved in self-control, as well as the hippocampus and thalamus. Meanwhile, blood flow increased around the visual cortex associated with food reward. All of this stimulated the foraging response.

"We believe that initially the fructose-dependent reduction in cerebral metabolism in these regions was reversible and meant to be beneficial," Johnson said. "But chronic and persistent reduction in cerebral metabolism driven by recurrent fructose metabolism leads to progressive brain atrophy and neuron loss with all of the features of AD."

Johnson suspects the survival response, what he calls the "survival switch," that helped ancient humans get through periods of scarcity, is now stuck in the "on" position in a time of relative abundance. This leads to the overeating of high fat, sugary and salty food prompting excess fructose production.

Fructose produced in the brain can lead to inflammation and ultimately Alzheimer's disease, the study said. Animals given fructose show memory lapses, a loss in the ability to navigate a maze and inflammation of the neurons.

"A study found that if you keep laboratory rats on fructose long enough they get tau and amyloid beta proteins in the brain, the same proteins seen in Alzheimer's disease," Johnson said. "You can find high fructose levels in the brains of people with Alzheimer's as well."

Johnson suspects that the tendency of some AD patients to wander off might be a vestige of the ancient foraging response.

The study said more research is needed on the role of fructose and uric acid metabolism in AD.

"We suggest that both dietary and pharmacologic trials to reduce fructose exposure or block fructose metabolism should be performed to determine if there is potential benefit in the prevention, management or treatment of this disease," Johnson said."
Please see original article with relevant diagrams and links here
h/t Marks Daily Apple here

Related Post
Link between Sugar and Alzheimer's - read it here

All the best Jan

Thursday, 23 February 2017

Diabetes could cause Alzheimer’s: Link between high blood sugar and dementia confirmed

EATING too much sugar could lead to Alzheimer’s disease - the most common form of dementia - experts have warned.

A diet high in sugar not only leads to diabetes and obesity but now researchers have revealed it can stop a protein from working efficiently.

Experts have confirmed there are biological links between dementia and high blood sugar.

Researchers at University of Bath compared brain samples of 30 people with and without Alzheimer’s disease and tested them for protein glycation, a modification caused by high glucose levels in the blood.

The team found that a particular enzyme was glycated in the brains of people with Alzheimer’s disease and that glycation stopped the enzyme from working properly.

The enzyme, known as ‘macrophage migration inhibitory factor’ or MIF, has been previously implicated in the inflammatory response that occurs in the brains of people with Alzheimer’s disease.

Dr Clare Walton, Research Manager at Alzheimer’s Society said: “We know that diabetes can double a person’s risk of developing dementia but we still don’t really understand how the two conditions are linked - this study offers a vital clue.

The researchers have found a specific effect of high blood glucose on an enzyme in the brains of people with Alzheimer’s, providing a plausible biological mechanism connecting the two conditions.

“With diabetes on the rise, a better understanding of how it affects brain cells can help us to find ways to help people with diabetes manage their risk of dementia.

“Alzheimer’s Society is currently funding a clinical trial to see whether a diabetes drug can be used as a dementia treatment.”

Professor Jean van den Elsen, from Bath's Department of Biology and Biochemistry, said: "We've shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer's disease. We are now investigating if we can detect similar changes in blood.

"Normally MIF would be part of the immune response to the build-up of abnormal proteins in the brain, and we think that because sugar damage reduces some MIF functions and completely inhibits others that this could be a tipping point that allows Alzheimer's to develop.

Dr Rob Williams, also from the Department of Biology and Biochemistry, added: "Knowing this will be vital to developing a chronology of how Alzheimer's progresses and we hope will help us identify those at risk of Alzheimer's and lead to new treatments or ways to prevent the disease.

Every week 4,500 people are diagnosed with diabetes across the UK.

Type 2 diabetes occurs when the body does not produce enough insulin or the insulin produced does not work properly.

The condition, which can be caused by being overweight and poor diet can cause blindness, limbs to be amputated and even kidney failure.


Reducing dietary carbohydrates is more effective in safely lowering blood glucose than any diabetes medications 

Graham

Thursday, 24 February 2011

Excess dietary carbohydrates and deficiency in dietary fats and cholesterol linked to Alzheimer's !

 
Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with alzheimer's disease, and may also be due in large part to this same underlying cause.
  
 
Recent population studies have confirmed a correlation between low blood serum cholesterol and both dementia and Parkinson's disease. A study published in 2007 compared three elderly population groups: subjects with dementia, subjects with depression, and controls. They found that those with dementia and depression had significantly lower serum cholesterol levels than the controls. Another study looking at Parkinson's disease among the elderly showed that those with the lowest LDL had 3.5 times the risk of Parkinson's disease compared to those with the highest serum LDL levels.

"Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease." 


 http://people.csail.mit.edu/seneff/EJIM_PUBLISHED.pdf


 

Thursday, 18 February 2016

"Alzheimer's = Type 3 Diabetes"

This article is by Mark Hyman MD.  


“My parents are getting older and I want to do everything I can to help them prevent Alzheimer’s, considering both my grandmothers had this disease, and I am worried about getting it too.” writes this week’s house call. “What can we do to prevent dementia?”

The truth is, dementia is a very big problem that’s becoming bigger every day.

Statistics are grim. 10 percent of 65-year-olds, 25 percent of 75-year-olds, and 50 percent of 85-year-olds will develop dementia or Alzheimer’s disease. And the fastest growing segment of our population is the 85-year-olds. Researchers predict Alzheimer’s will affect 106 million people by 2050. It’s now the seventh leading cause of death.

Scientists now call Alzheimer’s disease “Type 3 diabetes.” What’s the link between Alzheimer’s and diabetes? Well, new research shows Insulin resistance, or what I call daibesity (from eating too many carbs and sugar and not enough fat) is one of the major factors that starts the brain-damage cascade, which robs the memory of over half the people in their 80s, leading to a diagnosis of Alzheimer’s disease.

But don’t think too much insulin affects only older folks’ memories. It doesn’t just suddenly occur once you’re older. Dementia actually begins when you’re younger and takes decades to develop and worsen.

Here’s the bad news/good news. Eating sugar and refined carbs can cause pre-dementia and dementia. But cutting out the sugar and refined carbs and adding lots of fat can prevent, and even reverse, pre-dementia and early dementia.

More recent studies show people with diabetes have a four-fold risk for developing Alzheimer’s. People with pre-diabetes or metabolic syndrome have an increased risk for having pre-dementia or mild cognitive impairment (MCI).

You don’t have to have full blown type 2 diabetes to develop brain damage and memory loss from high insulin levels and insulin resistance.

We all have heard of the mind-body effect. Well, there is also a body-mind effect. So you can impact your brain through your diet and heal your body. In fact, your body and your mind aren’t two separate systems; they’re one elegant, continuous ecosystem. What you do to the body affects the brain, and what you do to the brain affects the body.

Cognitive decline and memory loss can be prevented and even reversed. We simply have to optimize brain function and then we see miracles. I’ve seen this happen many times in my medical practice.

The underlying causes of Alzheimer’s disease begin with too much sugar on the brain. The cycle starts when we over-consume sugar and don’t eat enough fat, which leads to diabesity. Diabesity leads to inflammation, which creates a vicious cycle that wreaks havoc on your brain.

If you looked at an autopsy of a brain of an Alzheimer’s patient, you’d see a brain on fire. This inflammation occurs over and over again in every chronic disease and very dramatically with the aging brain and overall aging process.

How to Reverse Memory Loss

The good news is you can reverse dementia and cognitive decline. To do that, you must control your insulin and balance your blood sugar levels, which will allow you to overcome diabesity and balance your mood, help your focus, help boost your energy level, and prevent all of the age-related brain diseases including Alzheimer’s."

You can read and see more here

You may also be interested in this recent article, by Jerome Burne " 
Prevention is the best way of tackling Alzheimer's. So why is it being ignored and dis-credited?" Read it here

 All the best Jan

Sunday, 27 February 2022

'Ketogenic diet as a metabolic treatment for mental illness'


"Ketogenic diets may be used to treat mental illness in the future

Adapted from Ketogenic diet as a metabolic treatment for mental illness by Nicholas G. Norwitz, Shebani Sethi Dalai, and Christopher M. Palmer.

Ketogenic diets have been used to treat drug resistant epilepsy in children for over one hundred years.

Now they are being used for other neurological conditions such as schizophrenia, depression, bipolar disorder and binge eating disorder.

There is strong evidence that common biological pathologies underlie these conditions such as abnormal glucose metabolism, neurotransmitter imbalances, oxidative stress and inflammation. These factors are all improved with a ketogenic diet.

Controlled clinical trials have shown improvement in:
Obesity, Type Two Diabetes, Multiple Sclerosis, Epilepsy, Alzheimer’s disease and Autistic Spectrum Disorder.

Uncontrolled clinical trials have shown improvement in:
Parkinson’s disease and Schizophrenia.

Case series and animal models have shown improvement in: Cardiovascular Disease, Binge eating disorder, Major Depressive disorder, Bipolar disorder and ADHD.

It is estimated that people who have mental illness live around 7 to 10 years less than those who do not have a mental illness. Sometimes this is due to suicide, but more often it is due to concurrent diabetes, heart disease, respiratory disease, infectious disease and cancer. All of these conditions are raised in people with mental illness. Sometimes this is due to poor health behaviours such as smoking or other lifestyle issues, and drug side effects can also cause problems. But even in people of a healthy weight and who are not on drugs, if they have mental illness, they are also more likely to have physical illness. Could switching the body and brain away from glucose use towards fat and ketone use improve matters?

Cerebral glucose hypometabolism and insulin resistance are features of Alzheimer’s disease, Parkinson’s disease, Schizophrenia, and Epilepsy. In one recent Cochrane review of epilepsy, as many as 55% of patients had complete remission of their fits on a ketogenic diet.

GABA/glutamate imbalance is a feature of Epilepsy and Schizophrenia. Oxidative stress is a feature of Schizophrenia, Bipolar disorder and Major Depressive Disorder. Oxidative stress and inflammation are mutually reinforcing processes. Major Depressive Disorder, Schizophrenia have these issues.

The Virta Health Group has demonstrated that a ketogenic diet is a well tolerated and effective strategy for treating type two diabetes. It reversed the condition in 54% of patients compared to 5% who received standard care. Alzheimer’s patients also improved on a ketogenic diet and also benefitted from medium chain triglyceride supplementation. (MCTs). Parkinson’s disease, Huntington’s disease and Multiple Sclerosis patients also showed improvement in studies. About 50 to 80% of patients with Alzheimer’s disease have cross over symptoms with schizophrenia, Bipolar disorder and major depressive disorder. These conditions all share common metabolic abnormalities.

It is thought that the ketogenic diet affects the gut microbiome and gut issues are thought to influence Autistic Spectrum Disorder. Two clinical trials reported sometimes complete symptom remission in patients with Childhood Autism when treated with a ketogenic diet.

Some case studies involve psychiatric patients who embarked on ketogenic diets for weight loss and gut problems, only to find a massive improvement in their mental conditions as well. Dr Christopher Palmer reported about an elderly woman with over 50 years of schizophrenia who was able to stop all her antipsychotic medication and has been symptom free for over 12 years. Another middle aged woman who had schizophrenia and depression went into complete remission and was able to get her degree and a full time job in the last four years. Both remain unmedicated and on their ketogenic diets.

Results with Binge eating disorder have also been impressive. These patients are usually on 20-30g of carbohydrate a day."

Words above taken from Diabetes Diet Blog here 
Full study can be read at Dr. P
erlmutter site here


As regular readers know, this blog is presented in a magazine style - we hope something for everyone. You will find a variety of articles, studies, thoughts, photographs, music and recipes!

However, not all the recipes ideas featured in this blog may be suitable for you. If you may have any food allergies, or underlying health issues these must always be taken into account. If you are a diabetic and not sure how certain foods may affect your blood sugars, test is best, i.e. use your meter.

All the best Jan

Friday, 17 May 2019

Link between Sugar and Alzheimer's





"The Startling Link Between Sugar and Alzheimer's 

A high-carb diet, and the attendant high blood sugar, are associated with cognitive decline.

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 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.”" 


Words above by Olga Khazan 

Related post:
Case Study Supports Keto As Treatment For Alzheimer’s disease - see more here 

All the best Jan

Friday, 28 September 2018

New Alzheimer’s report: The disease will double by 2060


This article is from Diet Doctor site written by Bret Scher, MD FACC he says:

"Alzheimer’s disease is perhaps the most feared diagnosis for all patients and their families. It doesn’t claim as many lives as heart disease or cancer, but its devastating effect on the lives of loved ones is immeasurable. For some, it is a fear worse than death. 

Unfortunately, the data surrounding Alzheimer’s is not encouraging. The Centers for Disease Control (CDC) released its estimate for the progression of Alzheimer’s Disease (AD) from 2015-2060. As of 2014, five million Americans, or 1.6% of all Americans, suffered from AD. The CDC predicts this number will increase to 13.9 million by 2060. 


Why will there be such a marked increase? One reason is simply the aging population. The other, however, is the explosion of chronic diseases such as diabetes (DM), insulin resistance (IR), and obesity, which may all play a role in the development of AD. In fact, an emerging name for AD is “Type III Diabetes.”  

Although that sounds discouraging, having AD related to insulin resistance and DM may turn out to be a good thing. After all, we are now learning that IR and DM are completely reversible. They are no longer the lifelong incurable diagnoses they were once thought to be. Interestingly, that is the same way we have always thought of AD. All too often doctors have said, “There is no good way to treat it or prevent it. Once you have it, it’s too late.” For that reason, some physicians even recommend against risk factor screening (i.e. with ApoE genetic testing), arguing “There is nothing to do to prevent it, so why would you want to know if you are at higher risk?” 

Fortunately for us, that mindset is starting to change. Starting with Amy Berger’s book, The Alzheimer’s Antidote, and Dr. Dale Bredesen’s book, The End of Alzheimer’s, we can now see a clear path to preventing and treating AD. But that path does not involve expensive drugs that have failed in trial after trial. 

Instead, the path to AD prevention and treatment may be the same as it is for DM, IR and obesity — low-carb nutrition, combined with an overall healthy lifestyle of regular physical activity, consistent sleep, stress management and other healthy practices. 

We hope to lead the way as you transform your health — and avoid an Alzheimer’s diagnosis down the line — with satisfying low-carb food.

Thanks for reading."

All the best Jan

Thursday, 16 April 2015

Statins Increase Your Risk Of Parkinson’s Disease By Up To 50%

Alzheimer’s disease and Parkinson’s disease are probably two of the most feared diseases, especially as we grow older. Both have devastating effects on the brain and nervous system and even though both diseases have “early onset” versions, generally they affect the elderly.
Now, a new study has found that you can cut your risk of Parkinson’s disease by 50 per cent if you avoid taking statin drugs… or viewed from a different angle: Statin drugs increase your risk of Parkinson’s disease by a whopping 50 per cent.
US researchers looked at blood cholesterol levels, medications and Parkinson’s disease status in nearly 16,000 men and women who participated in the ongoing, long-term Atherosclerosis Risk in Communities study. During the study, the researchers took cholesterol readings at three-year intervals over the course of a decade from 1987 to 1998, before widespread statin use began. Then, from 1998 to 2008, they tracked how many men and women had started statin therapy, and how many of them developed Parkinson’s disease.
The results showed that men and women who took statin drugs were twice as likely to develop Parkinson’s disease. But here’s the interesting part: The researchers linked higher total cholesterol with lower Parkinson’s disease risk.
Commenting on the study results, lead researcher Dr. Xuemei Huang, said, “If we blanket prescribe statins to people we could be creating a huge population of people with neurological problems.”
In fact, the study results even made waves in the UK. Dr. Kailash Chand, Deputy Director of the British Medical Association, said in an interview: “The risks of side-effects of these drugs are far greater than any potential benefits and it is high time these drugs were restricted…”
And he is right. Statin drugs have been linked to cataracts, type 2 diabetes, muscle damage, kidney and liver disorders, Alzheimer’s disease and memory loss, and even heart disease itself. And now we can add Parkinson’s disease.
For more than a decade we’ve been warning our readers against the cholesterol con. And now, finally, it seems like some mainstream doctors are beginning to cotton onto the truth: Our bodies produce cholesterol for a reason. It has an essential biological function and interfering with this natural biology has detrimental effects on our health.
A friend of mine recently used the following metaphor to describe the mainstream’s backward thinking when it comes to cholesterol: All cars have wheels. They need wheels in order to take us from point A to point B. However, cars are sometimes in accidents, which sometimes kill people. So what’s the solution? Take away their wheels, because without wheels they can’t make accidents, right?
Humans need cholesterol in the same way cars need wheels. It’s just how it works.
Graham