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Can Hot Chocolate Prevent Alzheimer’s?

Media Article - Drinking Hot Chocolate Could Prevent Alzheimer's


Alzheimer’s disease is a type of dementia that causes problems with memory, thinking and behaviour. The Alzheimer’s Association reports that one in ten people over the of age 65 and nearly half over the age of 85 have Alzheimer’s disease, with these numbers expected to gradually increase over time (Alzheimer's Association, 2013).

On 7 August 2013, the Daily Mail published online an article by Nick McDermott titled “Drinking hot chocolate could prevent Alzheimer's by boosting blood flow to the brain.” Despite the headline, the article reports on the potential benefits of drinking hot cocoa for those with impaired blood flow in the brain and other areas in which cocoa and dark chocolate have been shown to have beneficial effects. The focus of the article is a recent study which showed that elderly people with impaired blood flow in the brain, experienced improvement in blood flow and working memory as a result of drinking two cups of hot cocoa a day over a one month period.

Given the increasing prevalence of the disease, the severity of its impact upon not only the patient but those close to them, and the absence of a cure, the article was of significant interest. We were particularly interested in whether there was a scientific basis for the "almost too good to be true" headline.

Whilst the headline and summary are misleading and inaccurate, the article does provide an accurate description of the study undertaken, with sufficient information to make it clear that there is insufficient evidence to suggest that those with, or at risk of Alzheimer's disease, increase their consumption of hot chocolate or cocoa.

Neuroscientific Context


Dementia is a neurological disease which traditionally presents with cognitive disorders, ranging from small losses of memory to complete loss of long term memory, and eventually loss of body function. Almost all cases of dementia are associated with genetic mutations, and the disease is usually (but not always) late onset. Dementia is associated with a host of risk factors, such as age, head injury, education level and socioeconomic background. There are multiple types of dementia, with Alzheimer’s disease being the most common form. Typically patients with Alzheimer’s disease also present with a concurrent cerebrovascular disease.
Alzheimer’s disease is a neurodegenerative disorder which causes depreciation of both health and quality of life until eventual death (Guyton, 2011). Like all disease, Alzheimer’s is incredibly destructive, both in a pathophysiological and social context due to its severe, debilitating clinical manifestations. There is currently no cure for Alzheimer’s disease, and it can be indiscriminate of age, striking some individuals in their 30’s (Hassad & Phelps, 2011). However this form of Alzheimer’s disease, known as early onset Alzheimer’s, is very rare.

Alzheimer's Disease - the most common Dementia

Alzheimer’s disease was first described by Alois Alzheimer (although he did not name the disease), a German psychiatrist and neuropathologist. Alzheimer noted both the clinical manifestations and the histological signs on autopsy of his patient’s brain (Berrios, 1991). The term “Alzheimer’s disease” was coined by Emil Kraeplin, a colleague. The initial work of Alzheimer has been greatly expanded upon, leading to the modern hypotheses of the development and progression of Alzheimer’s disease.


A concrete mechanism for the cause of Alzheimer’s disease has not yet been found, however research has both discredited some common suspects and revealed several risk factors which are associated with increased risk of the disease. There is a strong suggestion that genetics play a role in the development of Alzheimer’s disease, as familial history is a risk factor (Hassad & Phelps, 2011). Alzheimer’s patients almost exclusively also have a history of or a concurrent neurovascular pathology (Hassad & Phelps, 2011).

Pathophysiology and Pathohistology

Grossly advanced Alzheimer’s disease displays diffuse atrophy of the brain, with more severe focal atrophy common in areas such as the hippocampus (Deutsch et al., 2012), a primary area involved with memory formation and processing (Guyton, 2011). The measurement of the rate of hippocampal atrophy is a strong defining indicator that the neural dementia is Alzheimer’s (Barkhof et al., 2009). This neural atrophy progresses with the symptoms of the disease, such as loss of memory and with progression general loss of cognitive function.

Figure 1: Coronal MRI scan comparison of a normal and Alzheimer’s disease brain:
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Figure 1: Generalised atrophy of the cortex and specific atrophy of the hippocampus, a defining marker of Alzheimer’s disease (indicated in bottom left image by arrow).

Source: Accessed 1/09/13

This atrophy is due to the death of cortical neural tissue, which in turn results in the loss of cholinergic innervation of the cortex, resulting in atrophy of associated cholinergic neurones in the forebrain (Barasi, Barker and Neal, 2008). The root cause of the cell death in the cortex is thought to be due to protein malformations that result in lesions of two major types: extracellular amyloid plaques and intracellular neurofibrillary tangles. The exact pathological process behind why these lesions cause atrophy is not well understood, however they have been recognised as significant factors in the disease process.

Post mortem microscopic analysis of the brain's of patients who suffered Alzheimer’s disease show these extracellular amyloid plaques and intracellular neurofibrillary tangles, in concurrence with synaptic degeneration and degeneration of the neurons of the hippocampus (Swerdlow, 2007). However, diagnostic criteria rely only upon the extent of extracellular amyloid plaques and intracellular neurofibrillary tangles, due to their consistent presence in the formation of Alzheimer’s disease.

Extracellular β-Amyloid Plaques

Extracellular amyloid plaques are build-ups of amyloid β-peptide, which is a fragment of the Amyloid Precursor Protein (APP), extracellular to the neuron. APP is a trans-membrane protein whose role in the nervous system is not yet fully understood, however it is has been found that leutinizing hormone regulates its production in post andropausal/menopausal patients (Atwood et al., 2004) which is being explored in respect to Alzheimer’s development and aging. Amyloid β peptide is cleaved off APP by the enzymes β and γ-secretase, and mutations in the γ-secretase and APP have been shown to be strongly linked to early onset Alzheimer’s disease (Hassad &Phelps, 2011).

Β-Amyloid plaques begin in both the limbic and hippocampal regions in Alzheimer's, and eventually progress to the cortex during later stages of the disease.

Figure 2: Bielschowsky stain highlighting beta-amyloid plaques in a brain section of Alzheimer’s patient
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Figure 2: A histological view of β-amyloid plaque in the hippocampus of a deceased patient. Note the extracellular nature of the plaque.


Intracellular Neurofibrillary Tangles

Intracellular neurofibrillary tangles are helical formations of hyperphosphorylated tau proteins that occur within the neuronal body. Tau protein, in its non-pathological neural function, serves as a stabilizer of microtubule proteins which neurons use to transport proteins from their nucleus down and across a synapse (Hassad &Phelps, 2011).

It is not yet understood if neurofibrillary tangles are a primary factor in the disease and its progression, or if they have a more peripheral role in its development.

Figure 3:
Bielschowsky Silver stain highlighting neurofibrillary tangles in a brain section from an Alzheimer's patient

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Figure 3: Histological view of tangles of Tau protein within a neuron. Note the intracellular nature of the tangle.


Treatment of Alzheimer's Disease

Alzheimer’s disease does not yet have a cure; however treatment is aimed at addressing the symptoms, such as memory loss and behaviour change. Drug treatments for memory loss include cholinesterase inhibitors such as Donepezil, which prevent the breakdown of acetylcholine. Other more ‘grass roots’ style options exist such as memory training games, dietary changes and lifestyle changes, all of which appear to have a beneficial effect.

Current Research into Alzheimer's Disease

Research into Alzheimer’s disease is fairly broad; however topics of focus seem to be around early detection methods, treatments and neurofibrillary tangles. A vast majority of research has been conducted in the past decade, with a large amount of it being reviews of hypotheses of disease pathogenesis. Many of these reviews offer new ideas for research, and are essential for furthering the scientific progress that will be made in the future (Schnabel, 2011).

The Role of Cocoa

One study in the US National Library of Medicine found that: ‘total cerebral blood flow was 20% lower in the AD group than in the NDC group, and that these values were directly correlated with pulse pressure and cognitive measures’. The NDC group refers to an age matched 'NonDemented Control' group. It is clear that associated with Alzheimer's disease are a range of cardiovascular diseases in the brain which lower the cerebral blood flow and lead to a decrease in cognitive activity. If the consumption of chocolate could improve cerebral blood flow it could help bring back some cognitive function.

The article reports that chocolate, or more importantly cocoa, a component of chocolate, has been linked to decreasing the effects of Alzheimer's disease. It is suggested that this activity is due to the high concentration of the anti-oxidant flavanoids that are found in cocoa. Upon further research, it appears that the specific anti-oxidant that is linked to improving cognitive function and decreasing the effects of Alzheimer's disease is Epicatechin. This particular anti-oxidant was first discovered in cocoa and is a flavan-3-ol. It has been found that cocoa contains ‘nearly twice the antioxidant content of red wine and up to three times that of green tea in vitro. ’

Figure 4: A representation of the chemical components of an epicatechin molecule.


Beta-amyloids create aggregates and lesions that coat the cerebral blood vessels along with Low-density Lipoproteins (LDL's) causing cerebral amyloid angiopathy or atherosclerosis. The plaques that form tighten the blood vessels leading to a decrease in blood flow through these vessels. Beta amyloid increase also leads 'to an increase in the production of endothelin converting enzyme-2, this converts a precursor to endothelin-1 which has been shown to act as a growth factor promoting the growth of plaques during AD' (Palmer et al, 2009). Another study showed that: 'Pure dietary flavonoids quercetin and (-)-epicatechin augment nitric oxide products and reduce endothelin-1 acutely in healthy men' (Am J Clin Nutr, 2009).

Epicatechin actively improves blood flow in two ways: firstly, by aiding in the breakdown of existing lesions in the blood vessels. Secondly, it slows the production of endothelin-1 which helps to stop the formation of new plaques.

Epicatechin and Antioxidants

One issue with antioxidants is that they have a relatively short half-life and break down within the body before they have sufficient time to circulate in the brain. This is where epicatechins are different. According to 'epicatechin is not broken down quickly in the body, and can get into the brain'. Through their longer half-life, epicatechins remain in the blood longer and can adequately aid in the break down of atherosclerosis lesions in the cerebral blood vessels. This puts them at a huge advantage in treating Alzheimer's disease as compared to other antioxidants from other sources.

By consuming more cocoa, the individual will have more of these beneficial anti-oxidants that can improve blood flow to the brain by lowering blood pressure and helping to clear plaques that build up in the brain.


The article comes from the website of the Daily Mail, a British tabloid newspaper. More than 1.6 million copies of the newspaper are sold each day, with 75% of readers over the age of 45 and just over half women
(, 2013). The newspapers website had over 8.2 million regular daily browsers in May this year
(, 2013), and despite the absence of a paywall, it is predicted that digital revenue could soon exceed print revenue
(, 2013). This indicates the paper’s target audience extends well beyond its traditional print based readers.

Whilst the website is littered with photographs of celebrities and sensationalist headlines, closer review reveals a mixture of articles, from those containing sophisticated content and analysis to sensationalised lightweight pieces. Despite a misleading and exaggerated headline and summary, the article being analysed falls into the former category and is authored by a journalist who specialises in writing science based articles.

The article includes a reasonable level of detail of the study undertaken, whilst not overburdening the average reader. It is clear that the author has read the journal article and he does a good job in accurately describing in layman’s terms the basic methods and results of the study, with minimal reference to scientific terms.

The fact the author has spoken with, and includes quotes from, the lead author of the study and other researchers in the field on both the findings and their clinical significance, serves to increase the articles accuracy and ensure that it does not overstate the research findings and their practical application clinically.

The author shows little apparent bias, making no real attempt to critically analyse the study. He presents a factual, balanced report on the study undertaken, its findings and their clinical significance, with brief comment on other areas in which cocoa has shown benefits.

On review of the entire article, there would appear to be substantial truth in the quote on the authors twitter page “I write the articles, not the headlines”, with the body of the article serving to mitigate the headline's misleading impression that the research is significant and will be successful in preventing Alzheimer’s disease. The headline/summary is not the result of the message being lost in translating complex findings into succinct layman’s terms, but rather a deliberate exaggeration of the importance and relevance of the study. The purpose of this is arguably to capture the attention and interest of those reviewing the website and increase the likelihood they will read the article, thereby generating traffic to the page on which the article is located and enhancing the newspapers ability to obtain online advertising revenue.

Whilst the misleading heading and summary facts fit with the all too common media portrayal of reported “breakthroughs” in the treatment of disease, the body of the article provides an accurate overview of the study, and makes it clear to the reader that more work needs to be done before it can be said that cocoa may prevent or be beneficial in the treatment of Alzheimer’s disease.


Our group was interested in finding out more about Alzheimer's disease and current research in the area., We came across the article selected in our search for media items dealing with Alzheimer's and the article's headline immediately caught our attention, as something which seemed "too good to true". Review of the article suggested that it was based upon a recent study and we decided that it would be interesting to analyse just how accurately the article reported the study's findings, whilst at the same time having the opportunity to learn more about current research in the area.

In undertaking research for the neuroscientific context section we attempted to focus on journal articles which had been widely cited and were from reputable journals. We also attempted to locate recent studies and take into account the research models used.

Reviewers of the draft version of the wiki identified the following as weak points of the wiki: inclusion of the full media article; missing references and a lack of referencing consistency; the absence of a section on treatment for Alzheimer's disease; repetition between a section in neuroscientific context and the analysis section; repetition in the analysis section; a lack of comment on current research; and suggestions that more detail be added to the section of neuroscientific context covering flavanoids. There were also general comments in respect of minor typographical and grammatical errors.

As a result of the feedback we made the following changes to the wiki: removed the media article and replaced it with a link; added a more obvious contents section; added in additional references and reviewed the wiki for referencing consistency; added information about current treatments for Alzheimer's Disease; edited and added additional information to the flavanoids section; edited and shortened the analysis section; removed the section from the neuroscientific context section which overlapped with the analysis section; and undertook a general review of the wiki for typographical and grammatical errors.


Alzheimer’s Association. (2013). What is Alzheimers?. Retreived September 1, 2013 from

Atwood,C.S., Bowen,R.L., Liu,T., Martins, R.N., Parlow, A.F., Perry, G., Smith, M.A., Verdile, G.(2004) Leutinizing hormone, a reproductive regulator that modulates the processing of amyloid-beta precursor protein and amyloid-beta deposition. Journal of Biological Chemistry, 279(19), 331-345

Barkhof, F., Barnes, J., Fox, N.C., Henemann, W.J.P., Scheltens, P., Sluimer,J.D., Sluimer,I.C., Van Der Flier, W.M., Vrenken,H. (2009) Hippocampal atrophy rates in Alzheimer’s disease-added value over whole brain volume measures. Neurology, 72(11),999-1007.

Berrios, G.E.(1991). Alzheimer’s Disease: a Conceptual History. International Journal of Geriatric Psychiatry, 5, 355-365.

Deutsch, G.K., Dougherty,R.F., Kerchner, G.A., Rutt, B.K., Saranathan,M., Zeineh,M. (2012) Hippocampal CA1 apical neuropil atrophy and memory performance in Alzheimer’s disease. Neuroimage, 63(1), 194-202.

Hall, J.E.(2011). Guyton and Hall Textbook of Medical Physiology. (12th ed). Philadelphia, PA. Saunders Elsevier 727-728

Ingram, M. (2013). The Daily Mail: Paywall? We don’t need no stinking paywall. Retrieved 31 August 2013 from

Palmer JC, Baig S, Kehoe PG, Love S.(2009). Endothelin-Converting Enzyme-2 is Increased in Alzheimer's Disease. America Journal of Pathology, 174, 2672-2680

Phelps K and Hassed, C.(2011). General Practice an Integrative Approach.(12th ed).Chatswood, NSW. Churchill Livingstone, 968- 971.

Press Gazette. (2013), Mail Online Sours To Biggest Ever Traffic Total with 129 million Unique Browsers Worldwide. Retrieved August 31 2013 from

Schanbel, J.(2011). Little proteins, big clues: after a quarter of a century, the amyloid hypothesis for Alzheimer’s disease is reconnecting to its roots in prion research. Nature, 475, 7355-7368.

The Daily Mail. (2013). Classified Fact Sheet. Retrieved August 31 2013 from, 2013

Image References:

Group Information

Ashleigh Lester z2272430
Jan Langejans z3253369
Rachel Cho z3369248
Stanley Rawlings z3481988

Division of Labour:
Rachel will handle the introduction and aims to be completed by Monday the 19th of August. Stanley, Ashleigh and Jan will divide the neuroscience and analysis between them with equal load on each. They aim to have the neuroscience context complete by 26th of August, and the analysis by the 2nd of September. We will then compile our appendix in the remaining week and plan to have a polished wiki page by the 9th of September.

As proof of our meeting we have included a photograph of our first group sit-down and discussion during which the above article and work report was decided upon.

Further meetings were held on: Thursday 5 September and Thursday 9 September.