As I have noted elsewhere (see HERE), the cause (or causes) of Alzheimer’s Disease is unknown at present. However, according to researchers, there are certain conditions, properties, or states of affairs that seem to raise the probability that a given individual will develop Alzheimer’s. These qualities, collectively and singly, are known as risk factors.

The biggest risk factors for getting Alzheimer’s are age (your chances increase as you get older) and genetics (especially if you’re a carrier of the ApoE4 gene). But there are others as well, for example having other diseases (like diabetes and Down’s Syndrome), conditions (such as atherosclerosis, high blood pressure, high cholesterol, and traumatic brain injury), or habits (chiefly, smoking) that predispose you toward dementia.

Preliminaries

Basics

Alzheimer’s is a neurodegenerative disease in which a person experiences drastic losses in cognitive abilities and memory. Patients suffering from it develop a bunch of “junk” in their brains – protein deposits of various sorts that conglomerate into abnormal structures referred to as “plaques and tangles” – that disrupts neural signals and kills off brain cells. These structures accumulate excessively and are not considered to be a part of the “normal” aging process.

“As in [normal] aging, widespread neuron loss and decreases in synaptic density are observed, though Alzheimer’s disease results in a significant preferential effect in the neocortex, hippocampus, amygdala, and basal nucleus of Meynert… Normal aging can result in the formation of plaques and tangles, but the amount and distribution does not compare to the brains of people with Alzheimer’s disease, in which greater quantities are common, especially in regions such as the temporal lobe.”[1]

• For more information on the general contours of the ailment, see my “What Is Alzheimer’s Disease? A Brief Overview.”

History

“The disease was first discovered in 1906 and described in a clinical journal article in 1907 by Alois Alzheimer, M.D. a German neurologist. He had first recognized the peculiar symptoms in one of his patients. a fifty-five-year-old woman. Dr. Alzheimer then referred to this disease in a published article as presenile dementia.

“Neurologists now agree that the dementia that occurs in the elderly is the same as or similar to the presenile condition. It is usually referred to today as senile dementia of the Alzheimer’s type (SDAT — more commonly leaving off the word ‘senile,’ medical specialists designate it just as DAT or Alzheimer’s disease).”[2]

• I have gone into much greater depth on the history of Alzheimer’s Disease elsewhere. For an introduction, see: “How Long Has Alzheimer’s Dementia Been Around?”

Cause(s)

Scientists have not yet determined a definite – let alone single – cause for Alzheimer’s Disease. Rather, there are a variety of postulated causes. These include the development of the previously mentioned plaques and tangles, sharp decreases in sex hormones (such as estrogen and testosterone) or neurotransmitters (like acetylcholine), chronic exposure to or excessive accumulation of toxins (e.g., aluminum or mercury), and so on.

• To read more in this vein, see: “10 Possible Causes for Alzheimer’s (& How to Address Them)”; “Can Drinking Alcohol Causes Alzheimer’s Disease?”; and “Can Contaminated/Dirty Tap Water Cause Alzheimer’s Disease?”

Risk Factors[3]

“Although an exact cause has not been identified, scientists have found several risk factors associated with Alzheimer’s disease. A risk factor predisposes someone to developing the disease. This means that someone with a risk factor is more likely to get a disease than someone without it.”[4]

“Risk factors for cognitive decline in aging are multifactorial, including medical co-morbidities and familial genetic risk.”[5]

Age

It turns out that, for everyone, the risk of developing Alzheimer’s goes up as we advance in years. This is repeated by numerous sources across the spectrum, from mainstream medical and scientific sources to more offbeat alternatives.

So, we read: “Age is the most important known risk factor for A[lzheimer’s] D[isease]. The number of people with the disease doubles every 5 years beyond age 65.”[6] And, again, alternative health guru Dr. Joseph Mercola states: “Your single greatest risk factor for Alzheimer’s disease is your age.”[7]

This is true as far as it goes. But there are other important factors. One is genetic.

Genes

“The gene apolipoprotein E-e4 (APOE-e4) has been identified as a …factor that most likely increases [the risk of] developing Alzheimer’s.”[8]

“Alzheimer’s disease is a neurodegenerative disorder mostly seen in the elderly. Presence of at least one apolipoprotein E4 (ApoE) allele is the strongest yet known genetic risk factor of late-onset Alzheimer’s disease. …Mutations of the genes encoding the [beta]-amyloid precursor protein and the presenilins 1 and 2 are risk factors for the early-onset form of Alzheimer’s disease. …”[9]

Family History

“Having a family history of dementia …[is] a risk factor for Alzheimer’s disease.”[10] Numerous studies have confirmed this.[11]

Contrariwise: “Subjects with A[lzheimer’s] D[isease] had a higher risk of having a family history of AD …as compared to control subjects.”[12]

Obesity

When a person is drastically more massive than is healthy for his or her height, the person might be said to be “obese.” “[A]ccumulating evidence links obesity to increased risk of Alzheimer’s and other types of dementia later in life…”.[13]

What is alarming – albeit somewhat intriguing – is that “[o]besity …[is] recognized as an important player in the pathogenesis of …dementia …independently of insulin resistance or other vascular risk factors.”[14] In other words, obesity isn’t just a factor because of increased risk of diabetes or hypertension or other factors listed elsewhere.

Sex

Is it possible that being female is actually an Alzheimer’s risk factor?

Indeed, one author reports: “It [has been] suggested …that female gender could act as a risk factor for Alzheimer’s disease…”.

However, researchers are unsure whether this is, in fact, a separate factor. The aforementioned writer goes on to state: “but it appears …that women are at higher risk because of their relatively increased longevity.”[15]

If this is the case, then really sex is itself not a distinct risk factor. It’s just that women are likely to outlive men. Since, as we’ve already said, the older a person gets, the greater his or her risk for Alzheimer’s, it follows that if women live longer than men, then they’ll be more likely than their male counterparts to get dementia.

Other Diseases

Furthermore, there are links between various other conditions and Alzheimer’s. “Some evidence points to risk factors similar to those for heart disease, including no physical exercised, high blood pressure and high cholesterol, a diet low in fruits and vegetables, and smoking.”[16]

Hardening of the Arteries (Atherosclerosis)

For example, there is a connection between “Alzheimer[‘s] neuropathology” and “atherosclerosis.” Atherosclerosis is termed a “vascular” disease because it afflicts the blood vessels of susceptible people. It’s sometimes referred to as a “hardening” of the arteries due to the fact that atherosclerosis involves gunk building up on the inside of those anatomical tubes.

These deposits are usually made of fat and, like their neurological cousins, are called plaques. One might get the impression that atherosclerosis and Alzheimer’s might both be characterized by the bioaccumulation of garbage inside the body.

From my point of view, this underscores the importance of living an overall healthy lifestyle, including getting adequate exercise and sleep as well as maintaining a proper diet. For more on some of these, see: “The Alzheimer’s ‘MIND Diet’: What Should You Eat?”; “Alzheimer’s and Sleep: Too Little, Too Much, and Just Right”; and “Alzheimer’s and Sleep: Herbs, Spices, and Other Supplements.”

However, it is worth noting that “atherosclerosis …[is] potentially reversible” and the link between it and dementia is far from being completely understood.[17]

Diabetes

In general, diabetes is a malfunction in a person’s ability to handle insulin, an essential, glucose-regulating hormone produced in the pancreas. This malfunction results in out-of-whack blood-sugar levels. There are two sorts of diabetes: Type 1 and Type 2. A person with the former must receive insulin from an external source, as his or her body produces little or none of it. Type 2 is generally regarded as less severe than Type 1, since a sufferer’s body is usually able to produce some insulin. Therefore, a Type-2 diabetic is not “insulin-dependent” in the same way as is a Type-1 diabetic.

“People with diabetes mellitus are at increased risk of cognitive dysfunction and dementia.”[18]

Down’s Syndrome

Down’s Syndrome is a genetic disorder. This condition arises when there is an extraneous copy of one chromosome (#21) in a parent’s (haploid) reproductive cells (gametes). This results in a sperm or egg cell with 24 chromosomes, instead of the usual 23. Combined with a normal gamete, the resulting offspring has 47 total chromosomes.

“People with Down’s syndrome …are at high risk for developing Alzheimer’s disease …at a relatively young age.”[19]

High Cholesterol (Hyperlipidemia; Hypercholesterolemia)

Cholesterol is a type of fat (or lipid) that is circulated in the body via the blood. It is produced by the liver and obtained in various foods (e.g., eggs). The body uses cholesterol to build new cells. So, having some of it is a good and necessary thing.

However, medical science is generally worried about the amount of cholesterol in your body. If it’s too high, the thinking goes, it can literally gummy up your blood vessels and increase your risk for cardiovascular and heart diseases.

Interestingly, “[s]everal lines of evidence have linked cholesterol to dementia.”[20]

Part of the reason for this may be because when blood flow is impeded, available oxygen can decrease. The brain is highly sensitive to oxygen deprivation. Hence, if the brain is not properly oxygenated, the deficit can cause damage that can lead to dementia.

High Blood Pressure (Hypertension)

Other “risk factors …[include] hypertension.” Because of this, and besides increasing “cognitive engagement,” researchers suggest that getting “regular physical activity …[, eating] the Mediterranean diet and …[consuming] omega-3 fatty acids …may reduce the risk of Alzheimer’s disease…”.[21]

Physical Brain Injury

There are also various external risk factors. “Head trauma …[is] is risk factor for Alzheimer’s disease…”.[22]

“Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer’s disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk.”[23]

This is a difficult factor to track precisely “[s]ince people with Alzheimer’s disease …[are] bound to have poor recollection of the exposure to head trauma…”.[24]

Aluminum

In discussions of environmental risk factors, the light metal Aluminum (Al) has been brought up repeatedly. It has been associated both with the development both of the beta-amyloid plaques and the tau-protein neurofibrillary tangles that are characteristic of Alzheimer’s-riddled brains.

One writer states “that even miniscule amounts of aluminum can boost the production of beta-amyloid” and that “aluminum seems to misfold tau [proteins], which would boost the risk of the typical tangles of Alzheimer’s.”[25]

“There has been suggestion of interaction between aluminum and several A[lzheimer’s] D[isease]-associated pathways.”[26]

This warning turns up in some rather unexpected places. Writing in his popular introduction on the ancient proto-science of Alchemy, Dennis Hauck writes as follows.

“Don’t use aluminum pots and pans or utensils when making alchemical products. Modern alchemists feel that aluminum metal acts as a kind of ‘energy sponge; that depletes spiritual energy. Several scientific studies seem to support the alchemists’ suspicions and have linked aluminum to mental retardation and Alzheimer’s disease.”[27]

• For more on heavy-metal and other kinds of environmental toxicity, see “Toxic Alzheimer’s? Household Hazards: Gases, Molds, Poisons” and “Household Hazards for People With Dementia.”

Smoking

Smoking is so strongly correlated with lung disease that the habit is believed to cause numerous health problems including chronic bronchitis, chronic obstructive pulmonary disease (COPD), emphysema, and even lung cancer.

Moreover, according to author Frank Murray, “smoking is definitely a significant risk factor for Alzheimer’s disease…”.[28]

Combined Risk Factors

Unsurprisingly, if factors are combined, then a person’s expected risk goes up. I won’t list all the various combinations, and I’m not a statistician. But, here are a couple of examples.

“Elderly people with type-2 diabetes have an 8.8 percent increase[d] risk of developing dementia, including Alzheimer’s disease.”[29]

Or, again: “Family history of Alzheimer’s disease and APOE-4 status [together] were associated with” several, physical brain abnormalities, including “a thinner cortex in the entorhinal region, subiculum, and adjacent medial temporal lobe subfields.”[30]

For Further Reading

• “Protect Yourself Against the coming Dementia Crisis”
• “10 Things to Do NOW to Reduce Your Risk of Alzheimer’s Later”
• “Top 25 Herbs for Treating (& Avoiding) Alzheimer’s Dementia”

Notes:

[1] Ronald Watson and Fabien De Meester, eds., Omega-3 Fatty Acids in Brain and Neurological Health, Amsterdam: Academic Press; Elsevier, 2014, p. 209, <https://books.google.com/books?id=HFgXAwAAQBAJ&pg=PA209>.

[2] Herman Richard Casdorph and Morton Walker, Toxic Metal Syndrome, New York: Avery; Penguin, 1995, p. 18, <https://books.google.com/books?id=7GJEveEcurMC&pg=PA18>.

[3] For more information, see Dementia: New Insights for the Healthcare Professional, 2011 ed., Atlanta: ScholarlyEditions, 2012, passim., <https://books.google.com/books?id=u89Efydxk7MC>.

[4] Linda Lu and Juergen Bludau, Alzheimer’s Disease, Santa Barbara, Cal.: ABC-CLIO, 2011, p. 16, <https://books.google.com/books?id=6gskihyGEQ0C&pg=PA16>.

[5] Lisa Morrow, Beth Snitz, Eric Rodriquez, Kimberly Huber, and Judith Saxton, “High Medical Co-Morbidity and Family History of Dementia is Associated With Lower Cognitive Function in Older Patients,” Family Practice, vol. 26, no. 5, Oct. 2009, pp. 339-343, <https://academic.oup.com/fampra/article/26/5/339/636444>.

[6] Eileen Welsh, ed., Frontiers in Alzheimer’s Disease Research, New York: Nova Science Publ., 2006, publisher’s blurb, <https://books.google.com/books/about/Frontiers_in_Alzheimer_s_Disease_Researc.html?id=dpMdC21dU9YC>.

[7] Joseph Mercola, Dark Deception: Discover the Truths About the Benefits of Sunlight Exposure, Nashville, Tenn.: Thomas Nelson, 2008, p. 71, <https://books.google.com/books?id=ay99sWUvTxoC&pg=PA71>.

[8] Jean Kaplan Teichroew, “Alzheimer’s,” Jean Kaplan Teichroew, ed., Chronic Diseases: An Encyclopedia of Causes, Effects, and Treatments, Santa Barbara, Cal.: ABC-CLIO, 2016, p. 53, <https://books.google.com/books?id=Am91DQAAQBAJ&pg=PA53>.

[9] Marcus Portallis, Focus on Hormone Replacement Research, New York: Nova Biomedical Publ., 2004, p. 87, <https://books.google.com/books?id=xWXSNNasBcEC&pg=PA87>.

[10] Ezra Susser, Sharon Schwartz, Alfredo Morabia, and Evelyn Bromet, with Melissa Begg, Jack Gorman, and Mary-Claire King, Psychiatric Epidemiology: Searching for the Causes of Mental Disorders, New York: Oxford Univ. Press, 2006, p. 367, <https://books.google.com/books?id=y6AN6bpfJhgC&pg=PA196>.

[11] See, e.g., D. Forster, A. Newens, D. Kay, and J. Edwardson, “Risk Factors in Clinically Diagnosed Presenile Dementia of the Alzheimer Type: A Case-Control Study in Northern England,” Journal of Epidemiology and Community Health, vol. 49, no. 3, Jun. 1995, pp. 253-258, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1060793/> and M. Rajah, L. Wallace, E. Ankudowich, E. Yu, A. Swierkot, R. Patel, M. Chakravarty, D. Naumova, J. Pruessner, R. Joober, S. Gauthier, and S. Pasvanis, “Family History and APOE4 Risk for Alzheimer’s Disease Impact the Neural Correlates of Episodic Memory by Early Midlife,” NeuroImage: Clinical, vol. 14, Mar. 31, 2017, pp. 760-774, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385589/ >.

[12] Ami Rosen, N. Kyle Steenland, John Hanfelt, Stewart Factor, James Lah, and Allan Levey, “Evidence of Shared Risk for Alzheimer’s Disease and Parkinson’s Disease Using Family History,” Neurogenetics, vol. 8, no. 4, Sept. 6, 2007, pp. 263-270, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2679377/>.

[13] Scott Kanoski, Ted Hsu, and Steven Pennell, “Obesity, Western Diet Intake, and Cognitive Impairment,” Ronald Ross Watson, Omega-3 Fatty Acids in Brain and Neurological Health, Amsterdam: Elsevier; Academic Press, 2014, p. 57, <https://books.google.com/books?id=HFgXAwAAQBAJ&pg=PA57>.

[14] L. Letra, I. Santana, R. Seiça, “Obesity as a Risk Factor for Alzheimer’s Disease: The Role of Adipocytokines,” Metabolic Brain Disease, vol. 29, no. 3, Feb. 20, 2014, pp. 563-568, <https://www.ncbi.nlm.nih.gov/pubmed/24553879>.

[15] Portallis, Focus on Hormone Replacement Research, loc. cit.

[16] Teichroew, “Alzheimer’s,” Teichroew, ed., Chronic Diseases, loc. cit.

[17] See H. Dolan, B. Crain, J. Troncoso, S. Resnick, A. Zonderman, and R. Obrien, “Atherosclerosis, Dementia, and Alzheimer [sic] Disease in the Baltimore Longitudinal Study of Aging Cohort,” Annals of Neurology, vol. 68, no. 2, Aug. 2010, pp. 231-240, <https://www.ncbi.nlm.nih.gov/pubmed/20695015>.

[18] Yael Reijmer, Esther van den Berg, Carla Ruis, L. Kappelle, and Geert Biessels, “Cognitive Dysfunction in Patients With Type 2 Diabetes,” Diabetes, vol. 26, no. 7, Aug. 26, 2010, pp. 507-519, <https://onlinelibrary.wiley.com/doi/10.1002/dmrr.1112>.

[19] Paula Castro, Shahid Zaman, and Anthony Holland, “Alzheimer’s Disease in People With Down’s Syndrome: The Prospects for and the Challenges of Developing Preventative Treatments,” Journal of Neurology, vol. 264, no. 4, Oct. 24, 2016, pp. 804–813, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5374178/>.

[20] A. Solomon, R. Sippola, H. Soininen, B. Wolozin, J. Tuomilehto, T. Laatikainen, and M. Kivipelto, “Lipid-Lowering Treatment Is Related to Decreased Risk of Dementia: A Population-Based Study,” Neuro-Degenerative Diseases, vol. 7, nos. 1-3, Apr. 2010, pp. 180-182, <https://www.karger.com/Article/Abstract/295659>.

[21] Yoram Barak, Preventing Alzheimer’s Disease: Personal Responsibility, New York : Nova Biomedical, 2014, publisher’s blurb, <https://books.google.com/books/about/Preventing_Alzheimer_s_Disease.html?id=tqiQvgEACAAJ>. Note that hypertension is also a risk factor for the second most common form of dementia, Vascular. See Sarah Jacobsen, Vascular Dementia: Risk Factors, Diagnosis, and Treatment, New York: Nova Science, 2011.

[22] Susser, Schwartz, Morabia, and Bromet, et al., Psychiatric Epidemiology, op. cit., p. 196.

[23] J. Hayes, M. Logue, N. Sadeh, J. Spielberg, M. Verfaellie, S. Hayes, A. Reagan, D. Salat, E. Wolf, R. McGlinchey, W. Milberg, A. Stone, S. Schichman, and M. Miller, “Mild Traumatic Brain Injury Is Associated With Reduced Cortical Thickness in Those at Risk for Alzheimer’s Disease,” Brain, Mar. 1, 2017, vol. 140, no. 3, pp. 813-825, <https://www.ncbi.nlm.nih.gov/pubmed/28077398>. In fact, the condition known as Dementia Pugilistica, previously referred to as “punch-drunk syndrome,” afflicts people — e.g., boxers and athletes involved in “contact” sports such as football/gridiron, hockey, martial arts, rugby, and wrestling — who experience damage to or disease of the brain due to repeated injury (such as blows to the head).

[24] Susser, Schwartz, Morabia, and Bromet, et al., Psychiatric Epidemiology, op. cit., p. 201.

[25] Jeffrey Victoroff, Saving Your Brain: The Revolutionary Plan to Boost Brain Power, Improve Memory, and Protect Yourself Against Aging and Alzheimer’s, New York: Bantam Books, 2003, p. 168, <https://books.google.com/books?id=M5SqLEYbWPAC>.

[26] A. Castorina, A. Tiralongo, S. Giunta, M. Carnazza, G. Scapagnini, and V. D’Agata, “Early Effects of Aluminum Chloride on Beta-Secretase mRNA Expression in a Neuronal Model of Beta-Amyloid Toxicity,” Cell Biology and Toxicology, vol. 26, no. 4, Jan. 29, 2010, pp. 367-377, <https://www.ncbi.nlm.nih.gov/pubmed/20111991>.

[27] Dennis Hauck, The Complete Idiot’s Guide to Alchemy, New York: Alpha; Penguin, 2008, p. 186, <https://books.google.com/books?id=SsolrTciALUC&pg=PA186>.

[28] Frank Murray, Minimizing the Risk of Alzheimer’s Disease, New York: Algora Publishing, 2012, p. 264, <https://books.google.com/books?id=9hveCHdjkt4C&pg=PA264>.

[29] Murray, Minimizing the Risk of Alzheimer’s Disease, op. cit., p. 255, <https://books.google.com/books?id=4f8Nj83E3R8C&pg=PA255>.

[30] Markus Donix, Alison Burggren, Nanthia Suthana, Prabha Siddarth, Arne Ekstrom, Allison Krupa, Michael Jones, Laurel Martin-Harris, Linda Ercoli, Karen Miller, Gary Small, and Susan Bookheimer, “Family History of Alzheimer’s Disease and Hippocampal Structure in Healthy People,” The American Journal of Psychiatry, vol. 167, no. 11, Aug. 4, 2010, pp. 1399-1406, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3086166/>.

12 Surprising Treatments for Alzheimer’s Dementia

Introduction

Straightforwardly, “treatments” are dietary or medical interventions that are tailored to address specific health deficits or pathologies. To state the obvious in plain English, when you think there’s a problem, you try to devise a solution. But Alzheimer’s is tricky because researchers are still in the position of having to guess about the root problem.

Elsewhere, I have catalogued “10 Possible Causes for Alzheimer’s (& How to Address Them).” At least in my own reading, these appeared to me to be among the most commonly mentioned hypothetical causes for the disease. They include the accumulation of beta-amyloid “plaques” and neurofibrillary “tangles,” a deficiency of the neurotransmitter acetylcholine, and an overabundance of the amino acid homocysteine, and other things.[1] (Click the above link for much more detail.)

In many ways, then, the “treatments” proposed in this article are geared toward the mitigation, relief, or reversal of one of more of the possible causes. Where relevant, I will note what cause is being addressed. But keep in mind that I have a fuller discussion of the causes and feel free to refer to it as needed or desired.

Also, understand that (most of) what follows in this article is probably best characterized with the heading “alternative” medicine. Readers who are interested in reding about more mainstream pharmaceutical recommendations can see my article HERE.

Caveats

Just a word or two of caution.

Firstly, I’m not a doctor. I’m not a dietician, either. Thus, the information presented here is given in good faith from my reflections on research that I have personally conducted. Usually, I will provide citations so that you can see and evaluate my source materials yourself. Basically, think of this article as giving you leads for your own follow-up investigations. I’m not trying to settle anything once and for all.

Secondly, and relatedly, many of the items on this list are highly controversial. Each of these has its vociferous proponents, and its equally vocal opponents. Again, I am not aiming to resolve these debates, here. In fact, by mentioning something, I’m not necessarily even endorsing it myself. My purpose is to make you aware of the lay of the land, options-wise.

Thirdly, in many ways, the treatments sort of “fall out” from a person’s views about the causes of Alzheimer’s. This means that certain readers might be more interested in some entries than in others simply because of what they believe about how Alzheimer’s begins or develops. But, at this time, the science is far from precise. So, there’s a sense in which the various options interconnect in complicated and sometimes interesting ways.

Twelve Surprising Treatments for Alzheimer’s

1.     Coconut Oil

In the introduction, I rehearsed a few of the best-known candidate causes for Alzheimer’s. However, there are others beyond the usual suspects. And here’s one of them.

Some people think that Alzheimer’s essentially results from energy deprivation in the brain. Those who take this line suggest that that cognitive impairment develops from a problem with the brain’s ability to use glucose.[2]

“In Alzheimer’s disease, brain cells have difficulty metabolizing glucose, the brain’s principal source of energy. …Ketone bypass the defect in glucose energy metabolism… Therefore, if enough ketones were available…, they could satisfy the brain’s energy needs. …”[3]

This bump in ketones occurs during fasting. But it can also come from ingesting a fatty acid called a “medium-chain triglyceride,” or MCTs. Wouldn’t you know it? Coconut oil is an important source.[4]

One author rhapsodizes that “…MCTs have produced better results in Alzheimer’s patients than any other treatment currently known to medical science. …The amount of MCTs in coconut oil is great enough to produce therapeutic blood levels of ketones.”[5]

2.     Sulphoraphane

Sulforaphane is an interesting one. Despite its somewhat forbidding name, it’s quite accessible, as it is a component of many green-leafy or cruciferous vegetables including some of the same offerings that were also rich in glutathione. Can you believe it?

It is a nutritional powerhouse that is credited with anti-inflammatory, antioxidant, and detoxification abilities. But it’s Alzheimer’s-fighting potential appears to go beyond these.

As discussed elsewhere, one feature of Alzheimer’s-afflicted brains is the appearance of various protein deposits – the aforementioned “plaques and tangles” – that interfere with neural activity and may also have a general neurotoxic[6] effect.

At least one scientific study suggested that sulforphane may actually “[inhibit] the generation and aggregation” of this debilitating gunk.[7]

3.     Glutathione

Another commonly cited potential cause for dementia is “oxidation” or “oxidative stress.” Some onlookers think that the accumulation of beta-amyloid plaques (and other features of Alzheimer’s) is a result of – or is at least bound up with – this oxidative damage.

Following this line of thought, “Studies …indicate that increasing the [body’s] antioxidative capacity through dietary or pharmacological intake of antioxidants can be beneficial in treatment of Alzheimer’s disease.”[8]

In this regard, glutathione has a reputation as a key antioxidant. In point of fact, glutathione is produced by our bodies. However, sadly, its “concentration” and production appear to decrease sharply with age. And increased “oxidative stress” may leave us more vulnerable to Alzheimer’s.[9]

What can be done?

Firstly, you need to think about your (or your loved one’s) diet. There’s really no getting away it. Computer scientists have a saying, abbreviated GIGO: Garbage in, garbage out. In their field, this has to do with a computer program’s sensitive dependence on what is entered in by the programmer. If the programmer types in “garbage,” the program may be lousy. But think about how this principle can relation to our health.

You really can’t expect your body to behave optimally if you fuel it with junk food. So, lay off the alcohol, processed foods, and sugar.

In place of these, you’ll need a found of fruits and vegetables. Some are excellent glutathione boosters. These include Arugula (Eruca vesicaria), Bok Choy (Brassica chinensis), Broccoli (Brassica italica), Brussels Sprouts (Brassica gemmifera), Cabbage (Brassica capitata), Cauliflower (Brassica botrytis), Chard (Beta vulgaris vulgaris), Garden Cress (Lepidium sativum), Kale (Brassica sabellica), Mustard (Brassica rapa), Rapeseed (Brassica napus), and Watercress (Nasturtium officinale).

Additionally, foods such as Artichokes (Cynara scolymus), various berries – Blueberry (Vaccinium corymbosum), Goji (Lycium chinense), Raspberry (Rubus idaeus), Strawberry (Fragaria × ananassa) – Cacao/Cocoa (Theobroma cacao), Catalase, Coenzyme Q10 (CoQ10), Hydroxytyrosol (C₈H₁₀O₃), Olive (Olea europaea), Red Wine, and Spinach (Spinacia oleracea) all have propensities to fight oxidation.

Secondly, you need to ensure that you maintain a consistent and adequate exercise regimen and sleep schedule. (For some tips on the latter, see my articles HERE, HERE, and HERE.)

• For more dietary considerations, see: “The Alzheimer’s ‘MIND Diet’: What Should You Eat?”

4.     Green Tea

While we’re on the subject of antioxidants, here’s another one that should probably be singled out for special attention: Green Tea (Camellia sinsensis).

As stated, Alzheimer’s is possibly – even if partially – a result of biochemical oxidation in the body.[10]

Once again, diet is fundamental to protection of your body’s neurons.[11] At the very least you’ll want to keep your levels of Vitamin-B Complex, Carotenoids (including the previously listed Astaxanthin, Beta Carotene, Lutein, and Lycopene), and Polyphenols within their optimal ranges. From a dietary perspective, this will involve eating generous helpings of quality fruits (especially berries), grains, and vegetables.[12] But it may also involve choice beverages such as …wait for it …green tea!

The bottom line is this. Research suggests that “Green Tea polyphenols protect neurons against P[arkinson’s] D[isease] and A[lzheimer’s] D[isease].”[13] One of the most remarkable of these polyphenols is Epi-Gallo-Catechin Gallate (EGCG).[14]

Other nutritional supplements can be quite helpful as well, for instance Milk Thistle (Silybum marianum), Selenium (Se), Turmeric (Curcuma longa), and Vitamin C (Ascorbic Acid) – all of which help boost your natural glutathione levels. You can even supplement with glutathione directly.

Finally, bear in mind that numerous other substances have antioxidant qualities. Some of the better known of these include Alpha Lipoic Acid (ALA), Astaxanthin (C₄₀H₅₂O₄), Beta Carotene (C₄₀H₅₆), Beta Glucan (C₁₈H₃₂O₁₆), Lutein (C₄₀H₅₆O₂), Lycopene (C₄₀H₅₆), N-Acetyl-L-Cysteine (NAC), Resveratrol (C₁₄H₁₂O₃), Super-Oxide Dismutase (SOD), and Vitamin E (Alpha-Tocopherol).

• For more, see: “Top 10 Nutrient and Vitamin Supplements for Alzheimer’s”

5.     Herbs

This category has consumed a lot of my attention on AlzheimersProof.com. For one thing, herbal supplements are easily acquired.

True, there may be considerable variation in quality and potency among various suppliers. (You can always try your hand at growing your own.) Still, I think these have potential for being of great assistance when it comes to staving off – or slowing down – Alzheimer’s.

Because I have gone into much greater detail elsewhere, I will really only list a few of my top choices, here. But I couldn’t neglect these entirely, as they are clearly major players in the realm of “alternative” dementia treatments.

So here are my Top Five Herbs for Alzheimer’s. For my entire list of Twenty-Five, see HERE.

·       Gingko (Gingko biloba)

If you’ve read continuously down this far, then you’ve probably noticed the recurring theme of antioxidants. And this is carried further with these herbal supplements.

There is little doubt but that ginkgo is a key player in the Alzheimer’s fight. In fact, according to one source, ginkgo is “[c]urrently the most widely prescribed treatment for A[lzheimer’s] D[isease] and other dementias in Germany… [It] is believed to work by stimulating nerve-cell activity in the brain while also improving blood flow and perhaps protecting against further cell damage as an antioxidant.”[15]

·       Magnolia (Schisandra chinensis)

Scientific research suggests that magnolia fruit has “a protective role in N[eurological] D[iseasess], including …neurodegenerative diseases” such as Alzheimer’s. Magnolia has several “neuroprotective mechanisms” including the aforementioned “antioxidation, suppression of apoptosis [i.e., cellular death – Ed.], anti-inflammation, regulation of neurotransmitters,” and other helpful things including “modulation of brain-derived neurotrophic factor (BDNF) related pathways” which, as far as I understand has to do with possible nerve growth or regrowth.[16]

·       Rosemary (Rosmarinus officinalis)

Another heavy lifter, rosemary is another potent antioxidant that may actually have the ability “to inhibit neuronal cell death”.[17] That is amazing news for Alzheimer’s sufferers. In fact, rosemary is so powerful, it may also be effective even as an essential oil in aromatherapy![18]

·       Saffron (Crocus sativus)

Prized as one of the world’s most exotic – and expensive – spices, saffron is also being shown to possess remarkable neuroprotective abilities. For example, it “has been identified as a memory-enhancing agent” and it has also reportedly “demonstrated effective antioxidant[,] …anti-inflammatory[,] and antiamyloidgenic abilities.”[19]

·       Turmeric (Curcuma longa)

Turmeric is an absolute supplement steamroller. It is an inflammation-fighting machine. Used “[i]n traditional South Asian medicine, turmeric (curcumin) …relieve[s] …Alzheimer’s disease due to its anti-inflammatory and antioxidant properties.”[20] At least one study suggested that Indians who eat curry regularly have better cognitive scores (when tested on the Mini Mental-State Examination, for more on which see HERE) and lower risk for dementia.[21]

For MUCH more on herbal supplements, see any (or all) of the following articles:

• “25 Herbs for Treating (& Avoiding) Alzheimer’s”
• “6 Drugs That Treat Alzheimer’s and 20+ Alternatives”
• “How to Alzheimer’s-Proof Your Diet: Vitamin D & Other Nutrients”

6.     Hormones

Let’s take these one at a time.

·       Estrogen

“Abundant evidence implicates sex steroid depletion in postmenopausal women as a risk factor for the development of A[lzheimer’s] D[isease].”[22] Another set of authors writes that “estrogen …plays a significant neuromodulatory and neuroprotective role.[23] The numerous estrogenic effects in the brain include the modulation of synaptogenesis, increased cerebral blood flow, mediation of important neurotransmitters and hormones, protection against apoptosis [i.e., cell death – Ed.], anti-inflammatory actions, and antioxidant properties. These multiple actions in the central nervous system support estrogen as a potential treatment for the cognitive decline associated with Alzheimer’s disease…”.[24]

·       Melatonin

Similarly to glutathione, “[d]aily melatonin production decreases with age, and in several pathologies, attaining its lowest values in Alzheimer’s dementia patients.”[25] Surely, this is a pity, especially since some investigators argue that melatonin has the ability to mitigate the sort of “neurodegeneration” that is typical of “…Alzheimer’s disease …, Parkinson’s disease …, and ischemia / reperfusion injury to the brain, i.e., stroke.”[26] But, arguably, it’s no coincidence.[27]

·       Progesterone

A close cousin to estrogen in this regard, “…progesterone  …facilitates some forms of learning and memory” and has been suspected to be a factor in a particular mouse-centered “model of Alzheimer’s disease.”[28] The reduction of both females sex hormones – estrogen and progesterone – “appears to be a significant risk factor for the development of A[lzheimer’s] D[isease] in women.”[29] There is some hope that hormone-replacement therapies can help reduce this risk.[30]

·       Testosterone

There are a couple of things going on, here. Most obviously, since testosterone levels decrease as men age whereas Alzheimer’s risk increases, “some researchers [have] proposed a relationship between the development of A[lzheimer’s] D[isease] and reductions of T[estosterone].”[31]

But, relatedly, in men who possess the Alzheimer’s predisposing Apolipoprotein-E4 gene, there is a link between “reductions in testosterone” and “the development of the amyloid beta …and tau …proteins” that gunk of the brain by way of forming plaques and tangles.

Because of these observations, a few writers even make the bold and provocative (but probably unproven) claim that “…Alzheimer’s can be cured in its early stages and halted in in its later stages …primarily using testosterone.”[32] It’s something to keep your eye on.

7.     Lithium

First of all, lithium exhibits neuroprotective properties and may guard against neuronal “apoptosis,” that is, cell death.[33] Second, and relatedly, it may help to break up – or discourage the formation of – the plaques and tangles that are among the main indications of the presence of Alzheimer’s.[34]

Lithium can be obtained from various foods, including coffee, dairy (e.g., cheese and milk), eggs, grains (rice, wheat), kelp, legumes (beans, chickpeas, lentils, peas, soybeans), mushrooms (like the Groundwart, Thelephora vialis), seafoods (like lobsters, oysters, shrimp, and scallops), nuts (like pistachios), and miscellaneous other vegetables (e.g., cucumbers and nightshade plants such as peppers, potatoes, and tomatoes).

But lithium can also be added to your diet by way of supplementation. Like calcium, magnesium, and zinc, lithium comes in a variety of forms, such as aspartate,[35] carbonate, chloride, citrate, and orotate. Of these, at least one source’s recommendation was states as follows. “Studies that have compared lithium orotate to lithium carbonate have found that lower doses or lithium orotate can achieve therapeutic brain lithium concentrations while avoiding toxicity.”[36]

8.     Marijuana

Wow. Here’s a hot topic right now. I realize that there is something of a sharp divide on this one. I don’t really want to wade deeply into a political debate. So, let me try to keep things fairly neutral – if possible.

One author observes: “Research suggests that cannabinoids (which are potent antioxidants) might be especially useful in minimizing inflammatory responses in the brain itself, symptoms of which are believed to be key to many serious neurodegenerative diseases ranging from Alzheimer’s dementia, to Parkinson’s disease, to other related motor disorders…”.[37]

Another, apparently amateur, researcher (of questionable accuracy) nevertheless echoes this, writing: “The cannabinoids of Cannabis sativa are neuro-protective and anti-inflammatory.”[38]

9.     Nicotine

“Drugs acting at nicotinic receptors including nicotine itself have been tested as treatments for cognitive impairments, including those seen in Alzheimer’s disease, schizophrenia, and attention deficit hyperactivity disorder (ADHD).”[39]

One source relates: “In Alzheimer’s disease patients, attentional performance has been found to be significantly improved with nicotine…”.[40] This “significant” improvement was demonstrated, for instance, through various activities evaluated on an attention-focused assessment called the Conners’ Continuous Performance Test (CPT, 3^rd Ed.). Nicotine administered through a patch for nearly a month seemed to elicit “a true increase in response accuracy”.

Another flatly states: “Nicotine treatment significantly improves cognitive function in people with mild-to-moderate Alzheimer’s disease.”[41]

10. Omega-3 Fatty Acids

This should be another dietary addition. Omega 3s are anti-inflammatory. “In addition, clinical studies have reported …the efficacy of omega-3 fatty acid in patients with attention-deficit hyperactivity disorder …, neurodegenerative disease such as Alzheimer’s disease …, and psychiatric disorders such as depression…”.[42]

Some randomized, controlled trials suggest that “omega-e …supplementation, particularly DHA, reverse age-related cognitive decline in otherwise healthy individuals… but these is less evidence to suggest such an effect in individuals with mild cognitive impairment and Alzheimer’s disease.”[43]

Still, “[e]pidemiological studies have shown that omega-3 fatty acid consumption reduces the risk of dementia… especially Alzheimer’s disease.”[44]

But, you need to watch the sort of fats that you eat. Overindulgence in saturated fats leads “to an increased risk of mixed dementia.”[45]

Some of the best sources include Cod-Liver Oil, Fish Oil, Flaxseed Oil, and Krill Oil.[46]

• For more extensive treatment of omega 3s, including my list of the best dietary sources, see the following: “The Alzheimer’s Dementia ‘MIND’ Diet: What Should You Eat?,” “Alzheimer’s-Proofing Your Diet: Carbs, Fats and ‘Exotics’,” and “Top Ten (10) Nutrient & Vitamin Supplements for Alzheimer’s.”

11. Red Wine/Resveratrol

Resveratrol, one of the active ingredients in red wine, is sometimes touted as an “anti-aging” drug.[47]

One of the telltale features of Alzheimer’s is the presence in the brain of the hardened plaques and tangles – mentioned elsewhere in this article and on my website – that interfere with neuronal activity and seem to “kill off” portions of the brain. Some researchers maintain that “[r]esveratrol is useful is stimulating the break-down [sic] of beta-amyloid peptides… In a study involving laboratory animals …who were given resveratrol from 45 days, there was a 45% reduction in plaques in the medial cortex, 89% in the stratum, and 90% in the hypothalamus.”[48]

Of course, with alcohol, one must remember the word moderation. (Some research seems to indicate that cognitive impairments can be precipitated by overindulgence. See HERE.)

Another thing to keep in mind is that not all wines are equal in their potential health benefits. Red wines tend to be healthier than white, and dry wines tend to edge out their sweeter counterparts.

Some of the red wines that often recommended include: Cabernet Sauvignon, Madiran, Malbec, Merlot, Petite Sirah, Pinot Noir, Rosé, Shiraz/Syrah, St. Laurent, and Zinfandel. Of these, three that stand out for resveratrol content seem to be Malbec, Pinot Noir, and St. Laurent.

• For more on wines and Alzheimer’s, see HERE.

12. Vitamins

As an untutored layman, one of the most surprising things to me in my reading about Alzheimer’s is its association with various deficiencies. I go into this more deeply in other places. (See HERE.) So I will limit myself to two examples, presently.

·       Vitamin B

“[C]ertain of the B vitamins …, when lacking or deficient in our diets, can …easily produce a loss of vital memory. …[T]here of them …[are]: vitamin B-1, or thiamin; B-3, niacin or nicotinic acid;[49] and B-12.”[50]

The esteemed Mayo Clinic relates: “Some studies suggest low vitamin B-12 levels may be associated with an increased risk of dementia.”[51]

·       Vitamin D

Vitamin D is another such vitamin. Once again, I will appeal to the Mayo Clinic, which states that some “[r]esearch suggests that people with very low levels of vitamin D in their blood …are more likely to develop Alzheimer’s disease…”.[52]

First of all, it has anti-inflammatory properties. And the devil of it is, is that we actually produce it ourselves if we get enough sunlight exposure.

Joseph Mercola relates this to the decrease in our bodies’ capabilities as we age. “The ability of your skin to produce vitamin D decreases the older you get, and vitamin-D deficiency has been shown to be common among those with Alzheimer’s.”[53]

• For a more in-depth discussion on vitamins, see my “Top Ten (10) Nutrient & Vitamin Supplements for Alzheimer’s” as well as my “10 Possible Causes for Alzheimer’s (& How to Address Them).”

A Few Concluding Remarks

Supplements – including the ones discussed here – are not supernatural. They cannot be expected to compensate for a lifetime of poor habits. So, firstly, I want to take a moment to reiterate the importance of what may be termed a “healthy lifestyle.”

Truly, diet and exercise are two indispensable keys to maintaining physical and mental fitness. In terms of nutritional guidelines, a good place to start is with the so-called Alzheimer’s “MIND Diet.” I have an entire article devoted to this topic, HERE.

Secondly, we are surrounded by environmental poisons and toxins and some of these severally – or possibly all (or some portion) of these jointly – may bear a measure of responsibility for dementias of one sort of other being as pervasive as they are. Therefore, part of your strategy needs to be minimizing your exposure, wherever possible. I have numerous posts on identifying and trying to eliminate these sorts of hazards.

These may include herbicides, metals, molds, pesticides, and myriad other things. For more information, see “Toxic Alzheimer’s? Household Hazards: Gases, Molds, Poisons” and “Home Contaminants and Hazards to Watch out For.”

For Further Reading[54]

• “Does Alzheimer’s Disease Have Three Stages or Seven Stages?”
• “Protect Yourself Against the Coming Dementia Crisis”

Notes:

[1] For the details, see my dedicated article.

[2] Bruce Fife, The Coconut Oil Miracle, New York: Avery; Penguin, 2013, p. 188, <https://books.google.com/books?id=aLS1nQEACAAJ&pg=PA188>.

[3] Fife, The Coconut Oil Miracle, op. cit., p. 190.

[4] For completeness, I note that “the administration of glucose has [also] been shown to improve cognitive function, for example, memory performance in Alzheimer’s …[i]n clinical populations with severe cognitive deficits…”. Veronika Schöpf, Florian Fischmeister, Christian Windischberger, Florian Gerstl, Michael Wolzt, Karl Karlsson, and Ewald Moser, “Effects of Individual Glucose Levels on the Neuronal Correlates of Emotions,” Michael Smith and Andrew Scholey, eds., Nutritional Influences on Human Neurocognitive Functioning, p. 129; reproduction of article from Frontiers in Human Neuroscience, vol. 7, no. 212, May 21, 2013; cached at <https://books.google.com/books?id=0wKlBQAAQBAJ&pg=PA129>.

[5] Bruce Fife, Ketone Therapy: The Ketogenic Cleanse and Anti-Aging Diet, Colorado Springs, Colo.: Piccadilly Books, 2017, pp. 103-104, <https://books.google.com/books?id=5dEwDwAAQBAJ&pg=PA103>.

[6] I.e., be poisonous to the brain or nervous system.

[7] T. Hou, H. Yang, W. Wang, Q. Wu, Y. Tian, and J. Jia, “Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer’s Disease (PS1V97L) Transgenic Mice,” Journal of Alzheimer’s Disease, vol. 62, no. 4, 2018, pp. 1803-1813, <https://www.ncbi.nlm.nih.gov/pubmed/29614663>.

[8] Nils-Erik Huseby, Elisabeth Sundkvist, and Gunbjørg Svineng, “Glutathione and Sulfur-Containing Amino Acids: Antioxidant and Conjugation Activities,” Roberta Masella, Giuseppe Mazza, eds., Glutathione and Sulfur Amino Acids in Human Health and Disease, Hoboken, N.J.: John Wiley & Sons, 2009, p. 112, <https://books.google.com/books?id=c9HznhSDlJAC&pg=PA112>.

[9] See, e.g., Ye Feng and Xiaochuan Wang, “Antioxidant Therapies for Alzheimer’s Disease,” Oxidative Medicine and Cellular Longevity, [vol. 2012,] Jul. 25, 2012, p. 472932, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410354/>.

[10] Baolu Zhao, “Green Tea Polyphenols Protect Neurons Against Alzheimer’s Disease and Parkinson’s Disease,” Lester Packer, Helmut Sies, Manfred Eggersdorfer, and Enrique Cadenas, eds., Micronutrients and Brain Health, Boca Raton: CRC Press; Taylor & Francis, 2009, p. 256, <https://books.google.com/books?id=ylX-GBKyLLkC&pg=PA256>.

[11] “Why is neuroprotection important? Neuroprotection refers to mechanism and strategies used to protect against neuronal injury, degenerative, or death in the central nervous system (CNS), especially following acute disorders such as stroke or traumatic brain injury or as a result of chronic neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and multiple sclerosis (MS)…”.

[12] Emma Ramiro-Puig, Margarita Castell, Andrew McShea, George Perry, Mark Smith, and Gemma Casadesus, “Food Antioxidants and Alzheimer’s Disease,” Packer, Sies, Eggersdorfer, and Cadenas, Micronutrients and Brain Health, op. cit., p. 43.

[13] Zhao, op. cit., in Packer, Sies, Eggersdorfer, and Cadenas, Micronutrients and Brain Health, op. cit., p. 257.

[14] L. Xicota, J. Rodriguez-Morato, M. Dierssen, R. de la Torre, “Potential Role of (-)-Epigallocatechin-3-Gallate (EGCG) in the Secondary Prevention of Alzheimer [sic] Disease,” Current Drug Targets, vol. 18, no. 2, 2017, pp. 174-195, <https://www.ncbi.nlm.nih.gov/pubmed/26302801>.

[15] Porter Shimer, New Hope for People with Alzheimer’s and Their Caregivers: Your Friendly, Authoritative Guide to the Latest in Traditional and Complementary Treatments, New York: Three Rivers Press; Crown Publ., 2002, p. 76, <https://books.google.com/books?id=wNli8hoE9TYC&pg=PA76>.

[16] Minyu Zhang, Liping Xu, and Hongjun Yang, “Schisandra chinensis Fructus and Its Active Ingredients as Promising Resources for the Treatment of Neurological Diseases,” International Journal of Molecular Sciences, vol. 19, no. 7, Jul. 6, 2018, p. 1970, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073455/>.

[17] Solomon Habtemariam, The Therapeutic Potential of Rosemary (Rosmarinus officinalis) Diterpenes for Alzheimer’s Disease,” Evidence-Based Complementary and Alternative Medicine, [vol. 2016,] Jan. 28, 2016, p. 2680409, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4749867/>.

[18] See Tadaaki Satou, Yuki Hanashima, Iho Mizutani, and Kazuo Koike, The Effect of Inhalation of Essential Oil from Rosmarinus Officinalis on Scopolamine‐induced Alzheimer’s Type Dementia Model Mice, Hoboken, N.J.: John Wiley & Sons, 2018.

[19] Nur Adalier and Heath Parker, “Vitamin E, Turmeric and Saffron in Treatment of Alzheimer’s Disease,” Antioxidants (Switzerland), vol. 5, no. 4, Oct. 25, 2016, p. 40, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5187538/>.

[20] Adalier and Heath Parker, loc. cit.

[21] Ibid.

[22] Jenna Carroll, Estrogen and Progesterone-based Hormone Therapy and the Development of Alzheimer’s Disease, dissertation, Univ. of Southern California, 2009, <http://digitallibrary.usc.edu/cdm/ref/collection/p15799coll127/id/177259>.

[23] Though, at least one offbeat and possibly unreliable author appears to argue that “estrogen causes Alzheimer’s.” If interested in the counterpoint, see Raymond Peat’s self-published Progesterone in Orthomolecular Medicine, Eugene, Ore.: Raymond Peat, 1993, <https://books.google.com/books/about/Progesterone_in_Orthomolecular_Medicine.html?id=XdQ6AgAACAAJ>.

[24] B. Cholerton, C. Gleason, L. Baker, and S. Asthana, “Estrogen and Alzheimer’s Disease: The Story so Far,” Drugs & Aging, vol. 19, no. 6, 2002, pp. 405-427, <https://www.ncbi.nlm.nih.gov/pubmed/12149049>.

[25] Daniel Cardinali, Analía Furio, and María Ryes, “Melatonin and the Cytoprotective Role of Sleep,” Pedro Montilla and Isaac Túnez, ed., Melatonin: Present and Future, New York: Nova Biomedical Publ., 2007, p. 175, <https://books.google.com/books?id=cQn9NNUinwYC&pg=PA175>.

[26] See Russel Reiter, Dun-Xian Tan, and Faith Gultekin, “Melatonin Reduces Molecular Damage and Physiological Dysfunction in Experimental Models of Neurodegeneration,” Montilla and Túnez, ed., Melatonin, op. cit., p. 261.

[27] Though, whether melatonin decline is a cause of Alzheimer’s or an effect from it is an open question.

[28] Michael Foy, Michel Baudry, Roberta Brinton, and Richard Thompson, “Estrogen, Progesterone and Hippocampal Plasticity in Rodent Models,” G. Casadesus, ed., Handbook of Animal Models in Alzheimer’s Disease, Amsterdam: IOS Press, 2011, p. 109, <https://books.google.com/books?id=vddRI_qV5_gC&pg=PA109>.

[29] Ibid., p. 110.

[30] See, e.g., William Fryer and M. Shippen, The Testosterone Syndrome: The Critical Factor for Energy, Health, and Sexuality — Reversing the Male Menopause, New York: M. Evans & Co., 2001, p. 149, <https://books.google.com/books?id=UdXwbE7fGiEC&pg=PA149>.

[31] Martine Simard, Séverine Hervouet, and Hélène Forget,“Testosterone Depletion and Cognitive Impairment in Aging Men: A Possible Relationship Between Testosterone and Alzheimer’s Disease?” H. Sentowski, ed., Cognitive Disorders Research Trends, New York: Nova Science Publ., 2007, p. 51, <https://books.google.com/books?id=0R3I_ZMZVW4C&pg=PA51>.

[32] Edward Friedman and William Cane, The New Testosterone Treatment: How You and Your Doctor Can Fight Breast Cancer, Prostate Cancer, and Alzheimer’s, Amherst, N.Y.: Prometheus Books, 2013, p. 19, <https://books.google.com/books?id=ybRvDwAAQBAJ&pg=PA19>.

[33] James Greenblatt, Integrative Medicine for Alzheimer’s: The Breakthrough Natural Treatment Plan That Prevents Alzheimer’s Using Nutritional Lithium, Fort St. Victoria, British Columbia (Canada): Friesen Press, 2018, p. 27, <https://books.google.com/books?id=GNx8DwAAQBAJ&pg=PA27>.

[34] Michael Bauer and Michael Gitlin, The Essential Guide to Lithium Treatment, Basel, Switzerland: Springer, 2016, p. 93, <https://books.google.com/books?id=ePg0DAAAQBAJ&pg=PA93>.

[35] Be wary of the aspartate form. According to Greenblatt (op. cit., p. 73) it may be linked to “excitotoxicity,” which is “[o]ne common pathway of numerous degenerative diseases…,” according to Julie Holland, The Pot Book: A Complete Guide to Cannabis, New York: Simon & Schuster, 2010, eBook, <https://books.google.com/books?id=tV0oDwAAQBAJ>.

[36] Greenblatt, Integrative Medicine for Alzheimer’s, op. cit., pp. 73-74. Note that, in the past (say late 1940s to early 1950s), some heart patients taking lithium chloride “developed lithium poisoning”, ibid., p. 38.

[37] Holland, The Pot Book, loc. cit.

[38] Joan Bello, The Benefits of Marijuana: Physical, Psychological and Spiritual, Susquehanna, Penn.: Lifeservices Press, 2008, p. 159, <https://books.google.com/books?id=J0cdQ_yn9aEC&pg=PA159>. The same writer further relates this interesting historical anecdote. “In 2737 BC[,] …Emperor Shen Nung compiled the first Chinese Pharmacopoeia. Marijuana was classified as one of the Superior Elixirs of Immortality. It was prescribed for absent-mindedness.” Ibid.

[39] David Balfour and Marcus Munafò, The Neurobiology and Genetics of Nicotine and Tobacco, Cham, Switzerland: Springer, 2015, p. 96, <https://books.google.com/books?id=00KMBgAAQBAJ&pg=PA96>.

[40] Melissa Piasecki and Paul Newhouse, eds., Nicotine in Psychiatry: Psychopathology and Emerging Therapeutics, Washington, D.C. & London: American Psychiatric Press, 2000, p. 207, <https://books.google.com/books?id=YXKzlaQ4zLgC&pg=PA207>. See, also, Paul Newhouse, A. Potter, and R. Lenox, et al., “Effects of Nicotinic Agents on Human Cognition: Possible Therapeutic Applications in Alzheimer’s and Parkinson’s Diseases,” Medical Chemistry Research, vol. 2, 1993, pp. 628-642.

[41] Balfour and Munafò, The Neurobiology and Genetics of Nicotine and Tobacco, loc. cit. This nicotine research appears to be in early stages. As nearly as I can tell, the nicotine affects “different attentional functions” by acting through “nicotinic acetylcholine receptor[s]” which seems clearly to tie this intervention in with other research on Alzheimer’s relation to acetylcholine deficiency, cholinesterase inhibition, and so on. For more, see HERE & HERE.

[42] Shogo Tokuyama and Kazuo Nakamoto, “Pain as Modified by Polyunsaturated Fatty Acids,” Ronald Watson and Fabien De Meester, eds., Omega-3 Fatty Acids in Brain and Neurological Health, Amsterdam: Academic Press; Elsevier, 2014, p. 131, <https://books.google.com/books?id=HFgXAwAAQBAJ&pg=PA131>.

[43] Grace Giles, Caroline Mahoney, and Robin Kanarek, “Omega-3 Fatty Acids and Cognitive Behavior,” Watson and De Meester, eds., Omega-3 Fatty Acids in Brain and Neurological Health, p. 322.

[44] Alyssa Velasco and Zaldys Tan, “Fatty Acids and the Aging Brain,” Watson and De Meester, eds., Omega-3 Fatty Acids in Brain and Neurological Health, op. cit., p. 212.

[45] Ibid.

[46] Evening Primrose Oil is a good source for the related Omega-6 fatty acids. But watch these! Too much of them can be problematic.

[47] <https://books.google.com/books?id=4f8Nj83E3R8C&pg=PA238>.

[48] <https://books.google.com/books?id=4f8Nj83E3R8C&pg=PA258>.

[49] To make matters more confusing, there’s also the related Nicotinamide, a.k.a. Niacinamide.

[50] Vernon Mark, Reversing Memory Loss: Medically Proven Methods for Regaining, Strengthening, and Preserving Your Memory, Boston: Houghton Mifflin, 1993, p. 100, <https://books.google.com/books?id=CbxMI-MCNm0C>.

[51] Jonathan Graff-Radford, “Vitamin B-12: Can it improve memory in Alzheimer’s?” Mayo Clinic, Oct. 14, 2016, <https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/expert-answers/alzheimers/faq-20057895>. For more, see Abram Hoffer and Harold D. Foster, Feel Better, Live Longer with Vitamin B-3: Nutrient Deficiency and Dependency, Toronto: Canadian College of Naturopathic Medicine Press, 2007.

[52] Jonathan Graff-Radford, “Vitamin D: Can it prevent Alzheimer’s & dementia?” Mayo Clinic, May 30, 2018, <https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/expert-answers/vitamin-d-alzheimers/faq-20111272>.

[53] Joseph Mercola, Dark Deception: Discover the Truths About the Benefits of Sunlight Exposure, Nashville, Tenn.: Thomas Nelson, 2008, pp. 71-72, <https://books.google.com/books?id=ay99sWUvTxoC&pg=PA71>.

[54] From a scholarly perspective, see Arrigo Cicero, Federica Fogacci, and Maciej Banach, “Botanicals and Phytochemicals Active on Cognitive Decline: The Clinical Evidence,” Pharmacological Research, Dec. 28, 2017, pp. 204-212, <https://www.ncbi.nlm.nih.gov/pubmed/29289576>.

Alzheimer’s is a neurodegenerative brain disease that, from the standpoint of symptoms, is characterized by the diminution of memory and reason. Usually it afflicts the elderly. (But there is also “early onset” Alzheimer’s that has impacted the lives of younger people.) Indeed, it used to be referred to as “Senile Dementia.”[1] For the time being, the exact cause of Alzheimer’s remains elusive. However, there are several physical / physiological signs that may point the way towards the articulation of a definitive statement about the condition’s cause(s) or etiology.

Many of these possible causes revolve around various observed defects (such as “beta-amyloid plaques” and “neurofibrillary tangles”) that present themselves in certain brain regions (e.g., hippocampus and cerebral cortex) of an Alzheimer’s-affected brain. Others have to do with detectable deficiencies (e.g., in neurotransmitters like acetylcholine, or in vitamins) or with the discovery of foreign substances (like bacteria and heavy metals) that deposit themselves in the brain.

For more information, read on.

Disclaimer

As I have stated elsewhere, I am not a doctor or medical professional of any kind. This article is based upon my own research. Where possible, I have quoted researchers who have far more expertise than I have. Nevertheless, readers should bear in mind that these possible cases have a hypothetical, speculative, or otherwise tentative quality. The precise cause (or causes) of Alzheimer’s is presently unknown. (See the bottom of the article for some additional provisos.)

Top Ten (10) Candidate Causes for Alzheimer’s

1.     Acetylcholine Deficiency

Biochemically, acetylcholine (C₇H₁₆NO₂) is produced by the body from the essential substance choline, which we may get from eggs, legumes, and soy. Functionally, acetylcholine is a neurotransmitter that helps our nervous system send impulses amongst neurons and between nerve and muscle cells.

For all the questions surrounding this disease, one thing researchers are fairly confident in is that “acetylcholine levels are abnormally low in people with Alzheimer’s”.[2]

It is by no means clear that the decrease in acetylcholine levels causes Alzheimer’s. It is perfectly compatible with the evidence that some other thing(s) causes both Alzheimer’s and the observed decrease in “cholinergic” (that is, acetylcholine-related neural) activity.

However, because of the correlation, numerous pharmaceutical and herbal interventions revolve around two, interrelated, strategies.

What can you do to increase acetylcholine levels?

Number one, doctors may try to increase the bioavailable levels of the relevant neurotransmitter. Straightforwardly, this is done by supplementing with acetylcholine or its precursor, choline.

And, number two, physicians may also try to stop the body from further breaking down the acetylcholine that it has. This is usually accomplished by trying to hinder, or inhibit, the action of the acetylcholine-dissolving enzyme cholinesterase.

Thus, there is a class of drugs called, appropriately enough, “cholinesterase inhibitors.” This class includes (or at one time included) such drugs as: Aricept (Donepezil), Cognex[3] (Tacrine), Exelon (Rivastigmine), and Razadyne (GalantamineListen). For more on these pharmaceuticals, see HERE.

Various herbs – such as Calamus (Acorus calamus), Clubmoss (Huperzia serrata), Cubeb (Piper cubeba), Gingko (Gingko biloba), Ginseng, Chinese (Panax ginseng), Juniper (Juniperus spp.) – may also display cholinesterase inhibiting properties. For much more on these (and other) herbs, see HERE.

2.     Homocysteine Levels High

Whereas acetylcholine levels are generally low in Alzheimer’s patients, the levels of other substances are found to be quite high.

For instance, various investigations suggest that “people with Alzheimer’s and other forms of dementia have higher levels of homocysteine in the blood than other people…”.[4] In fact, “[o]ne …study found that elderly people with high levels of …homocysteine have nearly twice the risk of developing the disease.”

Homocysteine is an amino acid. It’s presence is bound up with the biological processes whereby the body breaks down methionine (for more on which, see HERE) and the chemically related amino acid cysteine.

What can you do to decrease homocysteine levels?

It turns out that one of the most effective ways to lower homocysteine levels is to ensure that you have adequate amounts of the Vitamin-B Complex. Vitamins B-6 (Pyridoxine), B-9 (Folic Acid), and B-12 (Cobalamin) lower homocysteine levels.

Thus, out-of-control homocysteine levels could itself be caused by Vitamin-B deficiency. (See further.)

3.     Infection

This one may be a real shocker. And it comes in several variations.

One article in the magazine New Scientist had the stupefying title “Gum disease may be the cause of Alzheimer’s…”.[5] What?!

Here’s the deal. Several groups of researchers have discovered a particular bacterium, Porphyromonas gingivalis, in Alzheimer’s-affected brain regions.[6] This same bacterium is a common culprit in various gum inflammations (gingivitis) and gum infections (periodontitis).

It’s not clear how – or precisely when – the bacterium gets into the brain. It could be that poor dental hygiene enables bacteria to enter the bloodstream of otherwise healthy individuals and, ultimately, attack their brains. So, it could be a cause for Alzheimer’s.

On the other hand, it may only be “opportunistic”; the bacteria might simply take advantage of the fact that the brain of an Alzheimer’s patient is somehow more open to infection. This explanation might even be preferred since it seems plausible that dementia sufferers let their dental care slide.

Time – and additional research – may tell.

Another possible route for infection-to-Alzheimer’s comes from the Chlamydia pneumoniae bacterium. Unlike its sexually transmitted cousin, Chlamydia trachomatis, the former causes respiratory problems – including pneumonia.

In an autopsy-based study of around 30 brains – 15 with Alzheimer’s at death and 15 without – “[a]ll but one of the brains from Alzheimer’s patients were positive for C. pneumoniae; only one of the control brains was.”[7]

What can you do to counteract infections?

Firstly, you can try to ensure that you maintain good hygiene – both for yourself and your loved one. In terms of dental hygiene, this means brushing teeth after meals and flossing at least once per day. In general terms, it means observing good disease-mitigation practices around sick people. This involves washing hands correctly, covering mouths and noses when coughing/sneezing, properly discarding soiled tissues, not using “communal” towels, and disinfecting surfaces and dishes prior to use.

But, secondly, you should also ensure that your or your loved one’s diet and nutrition are optimal. This may include the observance of the so-called Alzheimer’s-friendly “MIND Diet,” about which you can read more HERE.

Thirdly, it is probably appropriate to seek advice or care from a competent medical professional. If the person is a modern medical practitioner, then he or she may prescribe one or more pharmaceutical antibiotics to address infections. These include: Amoxicillin, Azithromycin, Cephalexin, Ciprofolxacin, Clarithromycin, Doxycycline, Erythromycin, Penicillin, various Sulfonamides, and Tetracycline.

If the person is a naturopath or traditional healer, then he or she might recommend certain herbs – such as Bee Balm, Scarlet (Monarda didyma), Cat’s Claw (Uncaria tomentosa), Clove (Syzygium aromaticum), Echinacea (Echinacea purpurea), Garlic (Allium sativum), Ginger (Zingiber officinale), Goldenseal (Hydrastis canadensis), Oregano (Origanum vulgare), Sage (Salvia officinalis), Tea Tree (Melaleuca alternifolia), Thyme (Thymus vulgaris), Turmeric (Curcuma longa), and Uva Ursi[8] (Arctostaphylos uva-ursi) – and other substances – e.g., Honey – that have reputations as bacteria-fighters.

4.     Inflammation

We just mentioned gum inflammation. But inflammation can occur all over the body – including in the brain directly.

As it happens, “[i]nflammation in Alzheimer’s disease (AD) patients is characterized by increased cytokines and activated microglia.”[9] In fact: “Epidemiological studies suggest reduced AD risk is associated with long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs).”

These include over-the-counter offerings such as Aspirin (Bayer, Bufferin), Ibuprofen (Advil, Motrin), and Naproxen (Aleve, Naprosyn) and prescription-only drugs like Celebrex (Celecoxib), Feldene (Piroxicam), and Mobic (Meloxicam).

However, there may be other reasons why long-term NSAID use is not encouraged. For example, NSAIDS can cause damage to sensitive gut tissues and lead to ulcers.

What can you do about inflammation?

Thus, a person might wish to turn to alternatives, such as anti-inflammatory herbals. These include the following.

Basil (Ocimum basilicum), Black Pepper (Piper nigrum), Cardamom (Elettaria cardamomum), Cayenne Pepper (Capsicum annuum “acuminatum”), Cinnamon (Cinnamomum verum), Clove (Syzygium aromaticum), Frankincense, Indian (Boswellia serrata), Garlic (Allium sativum), Ginger (Zingiber officinale), Meadowsweet (Filipendula ulmaria), Nutmeg (Myristica fragrans), Rosemary (Rosmarinus officinalis), Sage (Salvia officinalis), Thyme (Thymus vulgaris), Turmeric (Curcuma longa), and White Willow (Salix alba).

You should also be aware that there are other supplements that can have an anti-inflammatory effect, such as Alpha Lipoic Acid (ALA), Bromelain – derived from the Pineapple (Ananas comosus) – Coenzyme Q10 (CoQ10), Fish Oil (Omega-3 Fatty Acids), Glutathione (C₁₀H₁₇N₃O₆S), Magnesium (Mg), Resveratrol (C₁₄H₁₂O₃) – derived from Red Wine, Spirulina (Arthrospira platensis and Arthrospira maxima), and Vitamins A (Retinol), B-6 (Pyridoxine), C (Ascorbic Acid), D (Ergocalciferol), E (Alpha-Tocopherol), K (Phytonadione).

Additionally, your general diet can allay inflammation. Focus on green, leafy and cruciferous vegetables such as Bok Choy (Brassica chinensis), Broccoli (Brassica italica), Brussels Sprouts (Brassica gemmifera), Cabbage (Brassica capitata), Cauliflower (Brassica botrytis), Chard (Beta vulgaris), Garden Cress (Lepidium sativum), Kale (Brassica sabellica), Spinach (Spinacia oleracea), Watercress (Nasturtium officinale). Other veggies can do you well also, including Tomato (Solanum lycopersicum). Don’t forget your berries – Blackberry (Rubus fruticosus), Blueberry (Vaccinium corymbosum), Raspberry (Rubus occidentalis), and Strawberry (Fragaria × ananassa). Additionally, you’ll want to add Olive Oil (Olea europaea) and Green Tea (Camellia sinensis). And, if you’re adventurous, you might spring for some mushrooms, including Maitake (Grifola frondosa) and Reishi (Ganoderma lucidum).

For more on dietary considerations for Alzheimer’s, see my article on the “MIND Diet,” HERE.

But the main point is that their seeming positive effect on Alzheimer’s risk suggests that inflammation is a major factor in the onset of dementia.

5.     Metal Poisoning (Aluminum, Copper, Lead, Mercury)

Let’s take these one at a time.

Aluminum

We’re continually exposed to this light metal. (For a more in-depth look at the sources of exposure to this metal, see my articles HERE and HERE.) And although it’s role in the development of various dementias is not entirely clear. Our sketchy knowledge is enough to raise concerns.[10]

For example, “[a]luminum seems to accumulate in the brain with age, and high levels of aluminum are found in the brains of victims of Alzheimer’s Disease.” The author then makes the obvious follow-up point that it is presently unknown whether the aluminum build up “is a cause or an effect of the disease”.[11]

Copper

Copper is a complicated metal to discuss because theorists are sharply divided over its role in Alzheimer’s Disease. On the one hand, there are those who speak about “copper therapy” as a means of addressing cognitive impairment. There is no question that copper is a micro- or “trace” nutrient that our bodies require in small amounts.

In small amounts. Note that phrase well. This reason?

“Too much copper …can cause a variety of ailments, including …severe damage to the central nervous system. …[H]igh levels of copper are also associated with …disorders, including …senile dementia (senility).”[12]

To read some more about the views on copper, see HERE and HERE.

Lead

Lead presents us with yet another case of how the various candidate causes on this list can dovetail. One journal article reports: “exposure to lead can potentially be implicated in Aβ and tau aggregation in AD”.[13] To translate: lead exposure might actually increase a person’s likelihood of developing the “beta-amyloid” Plaques and “tau”-protein-constituted neurofibrillary Tangles that are two major indicators of the presence of Alzheimer’s Disease. (For more on these, see their entry, below.)

Mercury

One author was convinced that mercury dental amalgams were capable of producing “[n]eurological …changes,” including the sorts of “sensory” problems that one sees in Alzheimer’s Disease.[14]

Besides his own stories, he points readers towards Tom Warren’s book Beating Alzheimer’s[15] for additional testimonial evidence.

Among the strongest statements that I located comes from Herman Casdorph and Morton Walker. Writing in their book, Toxic Metal Syndrome, they declare:

“Dental amalgams that allow mercury vapors to escape into the facial tissues, body, and/or brain cannot be excluded as a primary potential source of Alzheimer’s disease. …[T]here is no question that mercury vapor escapes with time from the surfaces of amalgams… There is definite evidence that mercury is shunted quickly from the blood and deposited in all organ tissues around the nervous system and brain.”[16]

The authors proceed to describe a study involving 22 autopsies – 10 performed on the brains of deceased Alzheimer’s patients, and 12 performed on non-sufferers functioning as the “control” group. The purpose was to catalog the prevalence of 13 “trace elements.”

The result?

The study’s authors stated: “[T]he elevation of mercury in …[Alzheimer’s] brains is the most important of the imbalances we observed. …This and our previous studies suggest that mercury toxicity plays a role in neuronal degeneration in Alzheimer’s disease.”[17]

Moreover, at least one pair of writers thought that mercury toxicity could be made worse when it occurred in the presence of other metals, chiefly copper and zinc.[18]

For more on possible sources of environmental mercury, including the aforementioned dental fillings, light bulbs (including compact-fluorescent and mercury-vapor), seafood (like tuna), and (some) vaccines, see my articles HERE and HERE.

What can you do about metal poisoning?

One common therapy for metal exposure is chelation. During chelation, certain substances are introduced into the body that form bonds with various metals, allowing them to be excreted.

Pharmaceutical-grade chelators include Ethylene-Diamine-Tetra-Acetic Acid (EDTA) – for lead and mercury; Di-Mercapto-Propane-Sulfonic Acid (DMPS) for mercury and Polonium-210; and Di-Mercapto-Succinic Acid (DMSA), for Arsenic (As), Lead (Pb), and Mercury (Hg). Glutathione (C₁₀H₁₇N₃O₆S) and Metallothionein (MT) are supposed to reduce levels of Arsenic, Cadmium (Cd), Lead, and Mercury. Additionally, Selenium (Se) is reportedly effective against Mercury as well. Transferrin is used to counteract Iron (Fe) poisoning.

Among the reputed alternative/herbal chelators are Chlorella (Chlorella vulgaris), Cilantro (Coriandrum sativum), Garlic (Allium sativum), Milk Thistle (Silybum marianum), and Spirulina (Arthrospira platensis).

Finally, various “Probiotics” (that is, “good” bacteria that live in your gut) – including Bifidus (Bifidobacterium longum), Acidophilus (Lactobacillus acidophilus), and Rhamnosus (Lactobacillus rhamnosus) – are possibly effective at reducing Cadmium and Lead.

6.     “Oxidative Stress”

Here’s the theory. “In the aging brain, as well as in the case of several neurodegenerative diseases, there is a decline in the normal antioxidant defense mechanisms, which increases the vulnerability of the brain to the deleterious effects of oxidative damage.”[19]

“Oxidative damage” is a bit obscure. In biochemical oxidation, some substance loses electrons. The most vivid example that I could find comes to us from everyday experience, rather than from biology. Iron turned into rust when it has lost electrons – that is, when it has been oxidized.[20]

Well, apparently, a similar change can occur inside of your body. There are some substances that can cause parts of your insides to “oxidize.” When this happens, if I understand correctly, the electrons are sort of carried around the body attached to particles typically called “free radicals.” These free radicals are unstable and are looking for something to react with. And the whole tangled business is, well… it’s bad, m’kay.

How bad? Well, some commentators suspect: “[A]ccumulated oxidative injury …results in many brain disorders including Alzheimer’s and Parkinson’s disease.”[21]

What can you do about oxidation?

Whether or not this amounts to a hard and fact causal connection, we can leave to the researchers to decide. But all this is one reason why I want to pepper my diet with oxidation-inhibiting substances called antioxidants. One of the best known of these antioxidants is good ol’ Vitamin C (Ascorbic Acid). (For more on this, see HERE.) I don’t know about you, but I’ll be loading up on the stuff.

Other fantastic (in the colloquial sense, of course) antioxidants are Beta-Carotene (C₄₀H₅₆), Lutein (C₄₀H₅₆O₂) and Lycopene (C₄₀H₅₆); Selenium (Se); Vitamin A (Retinol); Vitamin E (Alpha-Tocopherol); and Zinc (Zn).[22]

The hormone Melatonin (C₁₃H₁₆N₂O₂) is also reportedly powerful in this regard, as are Alpha-Lipoic Acid (ALA), Astaxanthin (C₄₀H₅₂O₄), Coenzyme Q10 (CoQ10), Glutathione (C₁₀H₁₇N₃O₆S), Methionine (C₅H₁₁NO₂S), N-Acetyl-Cysteine (NAC), Nicotinamide Adenine Dinucleotide (NADH),[23] and the enzyme Super-Oxide Dismutase (SOD).

From an herbal standpoint, Burdock (Arctium lappa), Catnip (Nepeta cataria), Cinnamon (Cinnamomum verum), Garlic (Allium sativum), Ginger (Zingiber officinale), Ginkgo (Ginkgo biloba), Grape Seed (Vitis vinifera), Green Tea (Camellia sinensis), Milk Thistle (Silybum marianum), Oregano (Origanum vulgare), Peppermint (Mentha × piperita), Pine, Maritime (Pinus pinaster),[24] Rosemary (Rosemarinus officinalis), Sage (Salvia officinalis), Spearmint (Mentha spicata), Thyme (Thymus vulgaris), Turmeric (Curcuma longa).

As usual, diet is extremely important. “[M]any antioxidants can be obtained from food sources such as sprouted grains and fresh fruits and vegetables…”.[25] Berries like Bilberry (Vaccinium myrtillus), Blueberry, Wild (Vaccinium angustifolium) and Goji Berry (Lycium chinense) and noteworthy. Pomegranate (Punica granatum) is also potent. The Pecan (Carya illinoinensis) and Walnut (Juglans nigra) should also get special mention. And, again, green vegetables pack a wallop. For a start, refer back to the list provided under Inflammation, above.

But, for much more information on dietary recommendations – including a more complete enumeration of fruits, grains, meats, and vegetables – that are specifically geared toward Alzheimer’s and other types of dementia, see my previous article on the “MIND Diet,” HERE.

7.     Oxygen Deficiency (“Hypoxia” & Ischemia)

Okay. Time for a few definitions. “Hypoxia” – meaning, roughly, under-oxygenated – has to do with states of oxygen deprivation. “Ischemia” refers to a state in which the brains (or heart’s) blood supply gets cuts off. This might occur because of a narrowing of the blood vessels. Or it might happen as the result of a blood clot (called a thrombus) “clogging” an artery or vein.

In any event, our organs need oxygen to live. It is unsurprising, therefore, that ischemia often precedes (or occurs alongside) infraction – which denotes the death of body tissue due to insufficient oxygen.

If brain tissue can literally die from lack of oxygen, though, there is little question but that “ischemia and hypoxia” sometimes “result in dementia” – including Alzheimer’s.[26]

One researcher[27] has opined that “cerebrovascular dementia is a matter of strokes large and small.”[28] This leads many to further insist that stroke-precipitated dementias “should be distinguished from Alzheimer’s disease…”.[29]

Regardless, oxygen deprivation can cause severe – and lasting – cognitive impairment.

One of the most intriguing pharmaceutical interventions is a substance known as Ergoloid (Hydergine). It was discovered (or developed, depending on how you view it) by Albert Hoffman of Sandoz. Recognize the name? He was also the man most associated with the hallucinogenic drug Lysergic acid diethylamide (LSD), often referred to as “acid.” In any case, Ergoloid is reputed to increase blood circulation and oxygenation. But it’s mechanisms of action are not well understood.

What can you do about oxygen deficiency?

Hypoxia can interrelate with other conditions, such as asthma or pneumonia. During acute, and identifiable, hypoxic episodes, a person suffering from hypoxia (or the related “hypoxemia,” when blood-oxygen levels are dangerously low) may require oxygen masks or other breathing apparatus. This is an emergency. During such an event, doctors or other hospital staff will keep tabs on oxygen levels and intervene as necessary.

In some cases, it may be appropriate to administer bronchodilators such as: Albuterol (Ventolin), Aminophylline (Euphyllin), Fluticasone (Flonase), Fluticasone & Salmeterol (Advair), Formoterol (Foradil), Ipratropium (Atrovent), Levalbuterol (Xopenex), Mometasone (Nasonex), Salmeterol (Serevent), Theophylline (Theochron), Tiotropium (Spiriva), and Vilanterol (Breo Ellipta).

Herbs sometimes employed in this context include: Asthma Plant (Euphorbia hirta), Cardinal Flower (Lobelia cardinalis), Chamomile, German (Matricaria chamomilla), Coneflower, Pale Purple (Echinacea pallida), Coneflower, Purple (Echinacea purpurea), Echinacea (Echinacea angustifolia) Guelder Rose (Viburnun opulus), Gumplant, Hairy (Grindelia hirsutula), Indian Coleus[30] (Plectranthus barbatus), Indian Tobacco (Lobelia inflata), Khella (Ammi visnaga), Licorice (Glycyrriza glabra), Ma-Huang (Ephedra sinica), Nettle, Stinging (Urtica dioica), Reishi (Ganoderma lucidum), Skullcap, Baikal (Scutellaria baicalensis), Sweetheart (Desmodium adscendens), and Thyme (Thymus vulgaris).

In more serious cases of respiratory distress, a physician might order an injection of Adrenaline (Epinephrine; EpiPen, etc.) – which is a both a hormone and a neurotransmitter – or some sort of oral steroid, like Dexamethasone (Decadron), Methylprednisolone (Medrol), Prednisone (Deltasone), or Prednisolone (Orapred).

Another possibly relevant concern is poor circulation. This can be addressed both proactively and therapeutically. Good eating habits are the foundation, here. This will include things like Oranges (Citrus X sinensis), as well as various kinds of fish, nuts, and red wine (in moderation). Since the Alzheimer’s-focused “MIND Diet” is based upon the heart-conscious “DASH Diet,” I invite you to see my main diet- and nutrition-related article, HERE.

However, be aware that supplements can be helpful. Some amino acids can be helpful, for example Arginine (L-Arginine), Carnitine (L-Carnitine), and Citrulline (L-Citrulline). Several vitamins and minerals are worth mentioning, also, including Magnesium (Mg), Vitamin C (Ascorbic Acid), and Vitamin D3 (Cholecalciferol).

Among the quality circulation-improving herbs are Barberry (Berberis vulgaris); Buckwheat (Fagopyrum esculentum); Garlic (Allium sativum); Ginger (Zingiber officinale); Ginkgo (Ginkgo biloba); Ginseng, Siberian (Eleutherococcus senticosus); Ginseng, Southern[31] (Gynostemma pentaphyllum); Goji Berry[32] (Lycium chinense) Guelder Rose (Viburnum opulus); Lotus, Sacred (Nelumbo nucifera); Motherwort (Leonurus cardiaca); Pepper, Cayenne (Capsicum annuum “acuminatum”); Pine, Maritime (Pinus pinaster); Prickly Ash, Common (Zanthoxylum americanum); Purslane, Common (Portulaca oleracea); Rhodiola (Rhodiola rosea); Sage, Red (Salvia miltiorrhiza); Turmeric (Curcuma longa); and Woflberry, Chinese[33] (Lycium barbarum).

8.     “Plaques & Tangles”

“The cause and progression of Alzheimer’s disease are not well understood. Research indicates that the disease is associated with plaques and tangles in the brain.”[34]

This, then, is the received view of Alzheimer’s, that one of its telltale signs is the presence of these “senile plaques and neurofibrillary changes,” including the so-called “tangles.”[35]

As mentioned in a previous section, the plaques are generally made up of something called “beta-amyloid” protein. And the tangles are composed of “tau” protein.

So, another author reports: “When we use a microscope to look at the brain of a deceased person who suffered from Alzheimer’s disease, two abnormal structures can be seen: amyloid plaques and neurofibrillary tangles. Some elderly people without dementia have small amounts of plaques and tangles in their brain. In Alzheimer’s disease, however, there are many. …[P]laques are most prominent in the brain regions that are important for memory, thinking, and decision-making. These regions include the hippocampus and temporal and parietal regions of the cerebral cortex.”[36]

It’s an open question whether these structures are the cause of Alzheimer’s, or whether they themselves are caused by some other factor.

What can you do about plaques and tangles?

Presently and officially? Not much. Unfortunately.

However, there are experimental drugs[37] being developed (e.g., Aducanumab) that attempt to break up plaques and tangles. Some question the rationale behind this, however, since it may take more than the mere dissolution of plaques and tangles to beat Alzheimer’s. After all, beta-amyloid plaques are preceded by Amyloid Precursor Proteins, or APPs. Without a mechanism or strategy for ridding the protein waste, some people worry that busting up plaques will simply scatter the beta-amyloid and “encourage” its reassembly.

Additionally, certain herbs hold out promise of having “antiamyloidgenic” properties, including Cat’s Claw (Uncaria tomentosa), Magnolia (Magnolia offincalis), and Saffron (Crocus sativus). Additionally, some scientists suggest that Sulforaphane (contained in broccoli) and Resveratrol (in red wine) might also possess anti-amyloid potential.

For a bit more on these possible interventions, see my “Top 25 Herbs for Treating (& Avoiding) Alzheimer’s” and “Top 30 (+5) Supplements for Alzheimer’s Detoxification.”

9.     Toxin Exposure (Chronic)

Once again, this overlaps with at least one previous category – that of Metal Poisoning (for which, see above). But it turns out that researchers are concerned that our toxic-exposure problems go beyond mercury fillings and tuna fish.

Another set of worries revolves around “mycotoxins” (or fungal toxins) and pesticides. In this regard, one investigator had the following to say.

“Recent evidence suggests that in utero or early life-exposure to certain pesticides, metals, and other environmental contaminants may cause neurodegenerative (Alzheimer’s, Parkinson’s, schizophrenia, Huntington’s, ALS, and others), metabolic, and cardiovascular diseases, and cancer later in life.”[38]

What can you do to “detox”?

There are numerous strategies that you can use to help cleanse and detoxify your (or your loved one’s) body. I have written an entire article on this.

For the information, see: “Top 30 (+5) Supplements for Alzheimer’s Detoxification.”

10. Vitamin Deficiencies

The lines between these various candidate causes sometimes blur. And this final category provides us with a final example of this.

When the brain is deficient in certain vitamins – for example, various components of the B-Complex – “oxygenation cannot occur” and this, in turn, can present symptoms similar “to those in patients with hypoxia”.[39]

Additionally, as has been stated previously, it’s by no means obvious which way (if any) the causal direction moves. So, while it is possible that vitamin deficiencies could cause Alzheimer’s, some authors take contrary positions.

For example, one writer states that “…Alzheimer’s disease patients may develop nutritional deficiencies, such as a lack of vitamin B1 (thiamine)…”.[40]

Other vitamins have been mentioned in connection with Alzheimer’s as well.

One author mentions that “vitamin C may …be important in preventing Alzheimer’s…”.[41]

Another warns: “There is strong evidence that links vitamin D deficiency to multiple sclerosis and a growing body of research associating it with Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis as well.”[42]

What can you do about vitamin deficiencies?

There are two primary and interconnected approaches. The first is to ensure (to the best of your ability) that you and your loved one are getting adequate levels of nutrients from your food. The basic starting point, here, is the so-called “Recommended Daily Allowances” (or RDAs)[43] that are established by the National Academy of Medicine.

Once again, I have a whole post just diving into this aspect of things. You can find that detailed dietary information, HERE.

Second, though, if there is a vitamin (or other) deficiency, then it might be appropriate to supplement with the vitamins that are lacking. I go into much more detail in “Top Ten (10) Nutrient & Vitamin Supplements for Alzheimer’s.”

A Few Summary Remarks

These Are Not the Only Candidate Causes

Although the ten possible causes just surveyed are among the most widely discussed, there are others that crop up in the literature from time to time.

For example, some investigators have observed (the fairly obvious fact) that Alzheimer’s risk increases with age. Well, some other things decrease with age, such as sex-steroid hormones (androgens, estrogens, and progestogens). So, some researchers posit a connection between dwindling levels of hormones such as estradiol, progesterone, and testosterone and Alzheimer’s Disease. Those who think this way may recommend hormone-replacement therapy (HRT) as an intervention.

Other authors try to pinpoint the cause of Alzheimer’s in an inability (in some people’s brains) to assimilate simple sugars and use them as energy. If this is so, it would suggest treatments such as the administration of glucose or alternatives. One alternative that has gained publicity recently is coconut oil.

For more on these, see my companion article: “12 Surprising Treatments for Alzheimer’s Dementia.”

Caveats

Genetic Caveat

After surveying the various, hypothetical causes, one might get a feeling of foreboding. It is possible that you might have a reaction similar to that voiced by the author of one of the source materials that I read.

He exclaimed: “After hearing all of this information, I wondered why we don’t all have Alzheimer’s.”[44]

And it’s a good question!

The answer could very well depend upon genetics. The major player, here, is the so-called “Apolipoprotein E,” abbreviated ApoE. It comes in three main variants: ApoE2, ApoE3, and ApoE4.

This isn’t the space to delve too deeply into this subject. But it’s worth considering that the various causal candidates – or some weighted sum of them – might only actually precipitate Alzheimer’s in a subpopulation that is predisposed to it in virtue of having one or more of these genes.

Philosophical Caveats

Here are a few important limitations to any discussion about causation.

Firstly, if we’re being technical about things in a philosophical sense, we should acknowledge that there is vast disagreement over what causality actually is[45] (and, for some thinkers, whether it exists or not[46]). This really isn’t the place to dive into this. Suffice it to say that the topic is a tangled one.

Secondly, it is a well-known logical-scientific maxim that establishing the existence of a correlation doesn’t settle questions about causation. Even if it’s true that every single Alzheimer’s sufferer whatever has lower-than-normal levels of acetylcholine (see above), that doesn’t demonstrate that acetylcholine deficiency causes Alzheimer’s.

A playful example can perhaps help to illustrate the point. Let’s stipulate that the following is true. For every single thunderstorm whatsoever, a barometer will register a decrease in air pressure. Even if this is universally true, it would be quite wrongheaded to conclude that the drop in air pressure (or that the barometer itself!) “causes” the thunderstorm. Thunderstorm development is a complicated interplay of moisture and air masses. (That’s the best I can do since I’m not a meteorologist!) This complex process involves a reduction in air pressure and, in turn, a falling barometer. But, arguably, these things are not correctly identified as causes of thunderstorms.

The moral: Correlation does not imply causation. So, be careful.

Thirdly, and relatedly, there are several ways that two things can be correlated. And although a few do deal with causation, the “causal direction” might not be quite what you would expect.

Consider two things, X and Y, that are strongly correlated, such that if X is present then Y is too and if Y is present then X is too. Still, any of the following could be the case.

X might cause Y. This is a possible explanation for the correlation. But, equally possibly (for all we know given only this evidence), Y might cause X. But it’s worse than this because it might turn out that both X and Y are both caused by some third, as as-yet unidentified, thing (Z). Finally, it could well be that X and Y merely happen to be correlated without any causal explanation.

Notes:

[1] The word “senile” comes from the Latin word senex, meaning “old man.”

[2] Carol Turkington and Deborah Mitchell, The Encyclopedia of Alzheimer’s Disease, New York: Facts on File; Infobase Publ., 2010, p. 64, <https://books.google.com/books?id=SA2X3ZHUZaEC&pg=PT82>.

[3] This drug is no longer used.

[4] Turkington and Mitchell, The Encyclopedia of Alzheimer’s Disease, op. cit., p. 43, <https://books.google.com/books?id=SA2X3ZHUZaEC&pg=PT61>.

[5] Clare Wilson and Debora MacKenzie, “Gum Disease May Be the Cause of Alzheimer’s – Here’s How to Avoid It,” New Scientist, Jan. 24, 2019, <https://www.newscientist.com/article/2191842-gum-disease-may-be-the-cause-of-alzheimers-heres-how-to-avoid-it/>.

[6] Ibid.

[7] Paul Ewald, Plague Time: How Stealth Infections Cause Cancers, Heart Disease, and Other Deadly Ailments, New York: The Free Press; Simon & Schuster, 2000, p. 125, <https://books.google.com/books?id=HlmxmE6TMCwC&pg=PA125>.

[8] Also called “Bear-Berry.”

[9] Bharat Aggarwal, Anushree Kumar, and Alok Bharti, “Therapeutic Potential of Curcumin Derived from Turmeric (Curcuma longa),” Lester Packer, Sissi Wachtel-Galor, Choon Nam Ong, Barry Halliwell, eds., Herbal and Traditional Medicine: Biomolecular and Clinical Aspects, New York: Marcel Dekker, 2005, p. 700, <https://books.google.com/books?id=UxBFTHxVXQwC&pg=PA700>.

[10] On how aluminum may “induce” neurofibrillary Tangles (for more on which, see their entry, above), see James Brown, Jr., Environmental and Chemical Toxins and Psychiatric Illness, Washington, D.C.: American Psychiatric Publ., 2002, pp. 103ff.

[11] Robert Ronzio, The Encyclopedia of Nutrition & Good Health, New York: Facts on File, 1997, p. 24, <https://books.google.com/books?id=1bzCYeHoJ8sC&pg=PA24>. For more on this, see: C. Exley, Aluminum and Alzheimer’s Disease: The Science that Describes the Link, Amsterdam: Elsevier, 2001 and Frank Murray, Minimizing the Risk of Alzheimer’s Disease, New York: Algora Publ., 2012.

[12] Phyllis Balch, Prescription for Nutritional Healing, 5^th ed., New York: Avery; Penguin, 2010, p. 350.

[13] Anne Kim, Sungsu Lim, and Yun Kim, “Metal Ion Effects on Aβ and Tau Aggregation,” International Journal of Molecular Sciences, vol. 19, no. 1, Jan. 2, 2018, p. 128, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5796077/>.

[14] Hal Huggins, It’s All in Your Head: The Link Between Mercury Amalgams and Illness, New York: Avery; Penguin, 1993, pp. 41-42, <https://books.google.com/books?id=7enhqv95boYC&pg=PA41>.

[15] Tom Warren, Beating Alzheimer’s: A Step Towards Unlocking the Mysteries of Brain Diseases, Garden City Park, N.Y.: Avery Pub. Group, 1991. See, also: Tom Warren, Reversing Chronic Disease: Getting Well Again, Washington, D.C. & Chula Vista, Cal.: Capital Univ. School of Integrated Medicine; New Century Press, 2004.

[16] Herman Casdorph and Morton Walker, Toxic Metal Syndrome, New York: Avery; Penguin, 1995, p. 156, <https://books.google.com/books?id=7GJEveEcurMC&pg=PA156>.

[17] Ibid., pp. 156 & 158. In other words, mercury came in first; bromine was second. The study tested for Bromine, Cesium, Chromium, Cobalt, Iron, Mercury, Potassium, Rubidium, Selenium, Silicon, Silver, Sodium, and Zinc.

[18] Hal Huggins and Thomas Levy, Uninformed Consent: The Hidden Dangers in Dental Care, Charlottesville, Virg.: Hampton Roads Publ., 1999, n.p., <https://books.google.com/books?id=ePkelycnYAEC>.

[19] Carmelina Gemma, Jennifer Vila, Adam Bachstetter, and Paula Bickford, “Oxidative Stress and the Aging Brain: From Theory to Prevention,” David Riddle, ed. Brain Aging: Models, Methods, and Mechanisms, Boca Raton, Fla.: CRC Press; Taylor & Francis, 2007, chap. 15; online at <https://www.ncbi.nlm.nih.gov/books/NBK3869/>.

[20] Oxidation is usually spoken of in tandem with “reduction,” which is the technical term for a substance’s gaining electrons. Therefore, some sources describe the overall reaction – where one thing gains the electrons lost by the other thing – a redox reaction.

[21] Tetsuya Konishi, Haruyo Ichikawa, and Hiroshi Nishida, “Protection of Oxidative Brain Injury by Chinese Herbal Medicine,” Lester Packer, Sissi Wachtel-Galor, Choon Nam Ong, Barry Halliwell, eds., Herbal and Traditional Medicine: Biomolecular and Clinical Aspects, New York: Marcel Dekker, 2005, p. 560, <https://books.google.com/books?id=UxBFTHxVXQwC&pg=PA560>.

[22] Man-made and chemical antioxidants such as Butylated Hydroxy-Anisole (BHA), Butylated Hydroxy-Toluene (BHT), and Propyl Gallate (Gallic Acid) are sometimes used in cosmetic- and food-preservative applications. Other compounds, like Tertiary Butyl-Hydro-Quinone (TBHQ), are employed in more “industrial” contexts.

[23] The missing “H” in the name has to do with the fact that NAD exists in both oxidized and reduced variants.

[24] This extract is sometimes marketed under the trademarked name “Pycnogenol.”

[25] Balch, Prescription for Nutritional Healing, op. cit., p. 65.

[26] See, e.g., Wilma Wasco and Rudolph Tanzi, Molecular Mechanisms of Dementia, Humana Press, 1997, <>.

[27] 20^th-21^st– century Canadian neurologist C. Miller Fischer. See, also: José Merino and Vladimir Hachinski, “Introduction: What Is Vascular Cognitive Impairment?” Olivier Godefroy, ed., The Behavioral and Cognitive Neurology of Stroke, Cambridge: Cambridge Univ. Press, 2013, p. 1, <https://books.google.com/books?id=s5FxQ_3SAwkC&pg=PA1>.

[28] Charles Gaitz, ed., Aging and the Brain: The Proceedings of the Fifth Annual Symposium Held at the Texas Research Institute of Mental Sciences in Houston, October 1971, New York: Plenum Press, 1972, p. 119, <https://books.google.com/books?id=zMtJAQAAIAAJ>.

[29] Gaitz, ed., Aging and the Brain, op. cit., p. 119.

[30] Also known as “Forskohlii.”

[31] Also called “Jiaogulan.”

[32] This is sometimes referred to as the “Chinese Wolfberry.”

[33] A.k.a. the “Matrimony Vine.”

[34] Samuel Barrack, Advances in Research and Treatment for Alzheimer’s Disease, London: iMedPub, 2012, blurb, <https://books.google.com/books/about/Advances_in_Research_and_Treatment_for_A.html?id=opDoR1LDACMC>.

[35] Gaitz, ed., Aging and the Brain, op. cit., p. 119.

[36] Sonja Lillrank and Christine Collins, Psychological Disorders: Alzheimer’s Disease and Other Dementias, New York: Chelsea House; Infobase Publ., 2007, pp. 48-49, <https://books.google.com/books?id=YJ_bMZhpuTYC&pg=PA48>.

[37] At various points, there has also been effort put toward the development of an anti-amyloid vaccine – e.g., UB-311. The idea, I think, it to try to elicit the body to attack plaques as they begin to form. However, this project does not appear to have had much success so far.

[38] Ramesh Gupta, Biomarkers in Toxicology, San Diego, Cal.: Academic Press; Elsevier, 2014, p. 4, <https://books.google.com/books?id=EMpUAgAAQBAJ&pg=PA4>.

[39] Gaitz, ed., Aging and the Brain, op. cit., p. 173.

[40] Casdorph and Walker, Toxic Metal Syndrome, op. cit., p. 18, <https://books.google.com/books?id=7GJEveEcurMC&pg=PA18>. He adds that this is often due to “routine, excessive, drinking of alcohol.” Ibid. Other writers speak as if Vitamin-B deficiency can be “Misdiagnosed Alzheimer’s.” On this, see Marie Mczak, The Secret of Staying Young: Age Reversal for Mind and Body, Twin Lakes, Wis.: Lotus Press, 2001, p. 19, <https://books.google.com/books?id=OtOVub6NH1AC>.

[41] Raquel Guine, Vitamin C: Dietary Sources, Technology, Daily Requirements and Symptoms of Deficiency, New York: Nova Science Publ, 2013, blurb, <https://books.google.com/books/about/Vitamin_C.html?id=BiXXngEACAAJ>.

[42] S. Roman and E. Monwry, “Vitamin D and the Central Nervous System: Development, Protection, and Disease,” Emilia Liao, ed., Extraskeletal Effects of Vitamin D: A Clinical Guide, Cham, Switzerland: Humana Press; Springer Intl., 2018, p. 232, <https://books.google.com/books?id=SYlXDwAAQBAJ&pg=PA232>. In yet a further case of interrelation, the author reminds readers that all four named conditions share certain features in common, such as “oxidative stress, inflammation, mitochondrial dysfunction, and cell death.” Ibid. Several of these have their own entries on this list.

[43] Also called “Dietary Reference Intake,” or DRI.

[44] Huggins and Levy, Uninformed Consent, n.p., loc. cit.

[45] Some people think of causation as nothing other than statistical correlation. On this view, saying “A causes B” is just to say that A and B are strongly correlated in some (particular) way. Others prefer what is called the “counterfactual” account of causality. On this picture, saying that “A causes B” means that if A hadn’t happened, then B wouldn’t have happened. There are many other perspectives.

[46] Those who believe that it does exist are sometimes referred to as causal realists. Those who disbelieve in it – at least, as its usually conceived – fall into either an antirealist camp (those who claim that “causal claims” are merely abstractions) or a nihilist camp (those who think either that there are no true causal claims or that there just is no such thing as “cause” at all).