Tuesday, 11 October 2011

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

For those who find reading full text papers difficult (why don't they use words more easily understood) they provide this useful summary of the main points.

Learning points
1. The amyloid-β present in Alzheimer's plaque may not be causal, since drug induced suppression of its synthesis led to further cognitive decline in the controlled studies performed so far.

2• Researchers have identified mitochondrial dysfunction and brain insulin resistance as early indicators of Alzheimer's disease.

3• ApoE-4 is a risk factor for Alzheimer's disease, and ApoE is involved in the transport of cholesterol and fats, which are essential for signal transduction and protection from oxidative damage.

4• The cerebrospinal fluid of Alzheimer's brains is deficient in fats and cholesterol.

5• Advanced glycation end-products (AGEs) are present in significant amounts in Alzheimer's brains.

6• Fructose, an increasingly pervasive sweetening agent, is ten times as reactive as glucose in inducing AGEs.

7• Astrocytes play an important role in providing fat and cholesterol to neurons.

8• Glycation damage interferes with the LDL-mediated delivery of fats and cholesterol to astrocytes, and therefore, indirectly, to neurons.

9• ApoE induces synthesis of Aβ when lipid supply is deficient.

10• Aβ redirects neuron metabolism towards other substrates besides glucose, by interfering with glucose and oxygen supply and increasing bioavailability of lactate and ketone bodies.

11• Synthesis of the neurotransmitter, glutamate, is increased when cholesterol is deficient, and glutamate is a potent oxidizing agent.

12• Over time, neurons become severely damaged due to chronic exposure to glucose and oxidizing agents, and are programmed for apoptosis due to highly impaired function.

13• Once sufficiently many neurons are destroyed, cognitive decline is manifested.

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

I've added the numbers so I can comment on them.
Re 1 We need to learn a lot more about Protein folding and if you want to help this research you can by downloading the computer program FOLDING HOME Whenever your PC is left on it works on this research project quietly in the background. My PC has completed 611 projects for them and I don't notice it working in the background and it's easy to pause if you want to play a game that requires 100% of you PC computing power.
2. Mitochondrial dysfunction is at the root of diabetes, metabolic syndrome and all that flows from these conditions. We can create new fully functional mitochondria by A)Exercise even modest exercise will help. B)Intermittent Fasting this does not have to mean a 24hr fast, Not eating between meals. Having just 2 meals a day, eating those 2 meals within 5hrs so there is 19hrs without any food. (gives a chance for fat burning) C) A Ketogenic diet. Less carbohrate more fat particularly coconut oil and Medium Chain Triglyceride oil. These are used as a substitute for glucose and metabolised straight away rather than being stored.
3.Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, including Alzheimer’s disease this full text paper will help you better understand the role of ApoE4.
4~ So we need more fats of the type that are known to be used in the brain, hence Coconut Oil, MCT, Butter (pasture fed higher omega 3) more OMEGA 3 fish oil less or no industrial seed oils like such as corn, soybean, safflower, sunflower and cottonseed oil and any commerially prepared food made using those pro inflammatory omega 6 oils.
5~ AGE's are the brown parts when foods are roasted/fried grilled and beginning to burn. Fewer roasts/barbeques/grills and more soups, stews and casseroles. Don't fry your bacon to a crisp. It's fine if it'slightly underdone. Liver tastes best if pink in the middle IMO.
6~ We shouldn't add HFCS to anything let alone baked items. This is particularly so when you buy baked items. It's just amazing where you find HFCS, corn syrup these days.
7~ For every brain neuron we have 10 times more astrocytes. Apart from providing ketones to keep neurones from starving should glucose sources get low, they also regulate blood flow through the brain. It's arguable disruption of brain blood flow is involved in MS. To keep astrocytes healthy they need feeding. Fat and cholesterol, bacon and eggs for breakfast fried in coconut oil. My choice for healthy astrocytes with a tsp of omega 3 fish oil.


  1. Excellent! First, it's so refreshing to have science explained in lay terms - thank you. Secondly, I've been searching for low-carb/paleo advice re aging, and like many others, Alzheimer's tops my list of concerns. Your advice re browning foods vs eating them slightly underdone is a great pointer - no more crispy bacon for me.

    I look forward to your next post.

  2. I'd forgotten I'd put this up.
    I've been posting at Alzheimer's UK website forum and blogspace, for some time but early month I'd got a warning from the moderators there that my posts were tantamount to "giving medical advice". So I thought I'd better shift some of my blogs to a safer place as I've been banned before from sites and then found all my stuff was unavailable to anyone and I wasn't able to rescue it.
    Anyway the danger past and then I was too busy to shift the rest here. But now you've reminded me I'll do so.
    I see from the blogs you follow we've a lot in common.

  3. This comment has been removed by the author.

  4. Hi Ted,
    What validity to give to theories that associate oxidative damage (not necessarily connected to ApoE-4) with the onset of dementia? Do you feel that antioxidant regimens can play any role in protecting against brain cell damage?