Can the course of early Alzheimer’s disease be delayed by consuming a special mixture of nutrients? This question was investigated in the European study called ‘LipiDiDiet’ led by Prof. Tobias Hartmann. 

The scientists recruited Alzheimer’s patients, who were in the early stages of the disease, to test the effectiveness of a specific nutritional drink called ‘Souvenaid’. Souvenaid was developed as a medical dietary food for the treatment of early-stage Alzheimer’s disease and is marketed by Nutricia (Danone Group). It contains a defined nutrient combination of long-chain omega-3 fatty acids, phospholipids, choline, B vitamins (B6, B12 and folic acid), vitamins C and E, selenium and uridine monophosphate. 

In this randomized double-blind study, the 311 participants were divided into two groups. The treatment group received the drink daily for breakfast. The control group was given daily  the same amount of a placebo drink, but with identical taste, consistency, color and calorie content. Neither patients, physicians nor researchers knew who was given the placebo or the multinutrient drink. 

The primary study endpoint was the slowing of cognitive decline. It was measured by a neuropsychological test battery, i.e., a combination of standardized cognitive testing procedures which measures not only the change in cognitive performance but also the ability to perform certain executive functions, such as planning, strategy and working memory. Furthermore, clinical aspects were also investigated using imaging techniques. Thus, structural brain changes could be directly recorded and assessed. 

Initial interim results after 24 months indicated some efficacy of the sip feed, but the differences in cognitive deterioration between the two patient groups were not significant. 

In September 2020, results after 36 months of treatment were published. They revealed significant differences between the two groups: Patients in the intervention group were measured to have 22 percent less brain atrophy, meaning that the brain mass of the treated Alzheimer’s patients had shrunk significantly less than that of the control group. Thus, the degenerative change process in the brain could be significantly slowed down by the nutrient preparation. In particular, the deterioration in the memory region of the brain (hippocampus), was 33 percent less in the treated patients than in the control group. It was also observed in regard to cognitive brain performance: it deteriorated 60 percent less, i.e. significantly less, in the treated subjects than in the no-treated patients.

Thus, the results of this study made it clear that such nutritional supplementation is not an effective concept in the short term. The effects seem to consolidate only with longer-term treatment, which was more than clearly shown by the comparison after 3 years with the interim results after 2 years. The researchers further found that the positive effects of the sip feed increased over the course of the treatment period and were not only focused on the memory region, but also extended to other cognitive areas. For example, the subjects were better able to cope with everyday challenges, such as paying bills, remembering routes, etc., than the control group.

This means that long-term intake of this specific multinutrient combination partially protects brain structures and reduces cognitive and functional decline in early Alzheimer’s disease. Thus, these nutrients appear to play a central role in reducing the neurodegenerative process in AD, suggesting a special nutritional need in AD. 

However, since it can be assumed that the disease begins decades before the first symptoms appear, but this cannot yet be measured with current methods, the timing to start therapy would also be crucial: the earlier, the better. Thus, not only the long-term duration of treatment would be important, but also the early start of treatment in the course of the disease. 

Despite intensive research, there is unfortunately still no medication that could cure Alzheimer’s disease. The currently available drugs can temporarily improve the symptoms, but let the patients fall back into the initial situation after some time. A sustained 3-year benefit of treatment, such as that achieved in this study with a defined nutrient mixture, has not yet been reported in incipient AD. With this in mind, the slower progression of the disease would already be a great success and is certainly a good start. 

These findings emphasize once again that AD is a generalized metabolic disorder in which monocausal therapies alone cannot lead to success, but multifactorial strategies must be used. And the international FINGER study (Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability) has already impressively demonstrated that multimodal prevention approaches can also pass clinical testing effectively. The ‘Souvenaid’ study is certainly a good start, as a sustained positive effect in terms of cognition, function and brain atrophy in an intervention for incipient Alzheimer’s disease has not yet been reported. Future studies could further clarify whether the efficacy of nutrient supplementation can be further enhanced if started at an even earlier stage, over a period longer than 3 years, as part of a multimodal intervention (e.g. FINGER trial) or in combination with pharmaceutical therapies.


The results of the aforementioned studies impressively underline that the multifactorial catalog of measures proposed by Knowledge stops Dementia – and especially a conscious diet that protects the brain – is the royal road in dementia prevention. It offers us a multitude of prevention strategies with which we can reduce our individual risk of Alzheimer’s disease by consistently minimizing avoidable risk factors and by adhering to a healthy lifestyle that includes not only nutrition but also other factors such as exercise, quality of sleep, social contacts, and so on. At the project ‘Knowledge stops Dementia’ you will find a lot more exciting and helpful information on this, so that you can maintain your mental health for as long as possible!


  1. Soininen H et al. (2017) 36-month LipiDiDiet multinutrient clinical trial in prodromal Alzheimer’s disease . Alzheimer’s and Dementia: 1-12 
  2. Soininen H et al. (2020) 24-month intervention with a specific mulitnutrient in people with predromal Alzheimer´s disease (LipiDiDiet): a randomised, double-blind, controlled trial. Lancet Neurol 16: 965–975 
  3. Ngandu T et al. (2015) A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. Lancet 365: 2255–2263 
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The fact that our health begins in the gut has been known for thousands of years. Today it is clear that our intestines are more than just a “digestive tube”, as this important organ fulfils a variety of other functions. For example, a disturbance of gut health is directly related to the development of chronic diseases.

 The intestinal flora, i.e. the microbial colonization of the intestinal mucosa, plays a particularly important role in this process. The intestinal flora is also known as the ‘intestinal microbiota’. It is the most important part of our immune system and thus offers us effective protection against infection.

But what few people know is that a correctly composed intestinal flora is also essential for our brain health, as it is directly connected to our nervous system via the intestinal-brain axis. An imbalance in the intestinal flora can lead to devastating consequences for the nerve tissue and in the worst case can cause neurodegeneration and dementia.

Alterations in the composition of the gut microbiota, caused by dietary changes, antibiotic exposure, and infection lead to the loss of the physiologic balance, which is implicated in the development of several diseases in humans, including Alzheimer’s disease. Recent evidence points to a causative link between changes in the intestinal microbiota composition, along with inflammatory changes in brain tissue. Hence, gut microbes may alter the level of neurotransmitter-related metabolites, affecting gut-to-brain communication and/or altering brain function.

Many studies on animal models have provided strong evidence of the importance of microbiota in the pathology of Alzheimer’s disease. Interesting results have been obtained, for example, with mice reared without intestinal microbial colonization and therefore without intestinal microbiota. These ‘aseptic’ mice showed an increased permeability of the blood-brain barrier (BBB) compared to mice with normal intestinal flora. This means that pathogens and other harmful substances from which the brain with an intact BBB is normally protected, are now able to enter the brain tissue. This can lead to an inflammatory reaction in the central nervous system called neuroinflammation, which is directly linked to the development of Alzheimer’s disease (see section causes for further information).

Such results obtained in animal models have also been confirmed by clinical studies:  For example, the intestinal microbiota of elderly people suffering from cognitive disorders was investigated, and an association between plaque deposits in the brain with the occurrence of pro-inflammatory intestinal bacteria and other inflammation markers could be shown.

In summary, all these results provide clear evidence that the effect of the intestinal microbiota on the development of the amyloid pathology may be significant and thus define its important role in the pathogenesis of Alzheimer’s disease.

But the good news is that our gut microbiota is a dynamically modifiable system that is very sensitive to lifestyle and ageing. With this knowledge, we can use a healthy lifestyle to positively influence our intestinal microbiota and develop practical recommendations for the prevention and treatment of Alzheimer’s disease.

Are you curious and would like to know more about this topic? 

To support the project ‘Knowledge stops Dementia’ ( the Academy of Human Medicine (AMM) has developed a fact sheet on dementia and intestinal health, which provides you with an evidence-based but compact overview of the above described relationships.

If you are interested in this fact sheet, it would be best to take part in the AMM’s current fundraising campaign for KSD.

Click here for the current AMM fundraising campaign… 

And don’t forget: healthy gut, healthy brain!

We thank you in advance for your support!

Your KsD team


  1. Vogt NM, Kerby RL, Dill-McFarland KA, et al. Gut microbiome alterations in Alzheimer’s disease. Sci Rep. 2017;7(1):13537.
  2. Harach T, Marungruang N, et al.  Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota. Sci Rep. 2017 Feb 8;7:41802. 
  3. Kowalski K, Mulak A. Brain-Gut-Microbiota Axis in Alzheimer’s Disease. J Neurogastroenterol Motil. 2019;25(1):48‐60. 
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The 2020 report of the Lancet Commission on Dementia Prevention, Intervention, and Care lists 12 modifiable risk factors that could help prevent dementia. This new report provides some important updates to the previous document, published in 2017.

The 2017 report had already recognized that acting on certain modifiable factors could help reduce a person’s risk of developing dementia. These factors are:

  • a lower level of education
  • hearing loss
  • hypertension
  • obesity
  • smoking
  • depression
  • low social contact
  • physical inactivity
  • diabetes

To the original nine factors, the new report has added 3 more:

  • head injuries
  • excessive alcohol intake
  • air pollution

Head injuries – Traumatic brain injuries are usually caused by car, motorcycle, and bicycle accidentes; military exposures; firearms; boxing, horse riding, and other recreational sports, most of them occurring during midlife. Falls are the most common cause of brain injuries later in life.

Excessive alcohol intake – Even though it has been previously shown that low doses of alcohol can prevent cardiovascular diseases, heavy drinking is associated with brain changes, cognitive impairment, and dementia – a risk known for centuries. Drinking more  than 21 units of alcohol per week (1 unit of alcohol=10 ml or 8 g pure alcohol) is  associated with a high  risk of dementia. 

Air pollution – Airborne particulate pollutants accelerate neuro- degenerative processes through cerebrovascular and cardiovascular disease, Aβ deposition, and amyloid precursor protein processing. High nitrogen dioxide (NO2) concentration, fine ambient particulate matter (PM)  from traffic exhaust and PM  from residential wood burning are associated with increased dementia incidence.

Together, the 12 modifiable risk factors account for around 40% of worldwide dementias, which consequently could theoretically be prevented or delayed. 

It is clear that the contribution of risk factors to the development of dementia begins early and continues throughout life, so it is never too early or too late to initiate any measures that will mitigate the negative effect of the 12 risk factors. Changes in any risk factor alone can prevent or delay dementia symptoms and should always be encouraged.

What can be done?

Preventive actions require both policy and individual engagement. Public health programs should be developed to increase social, cognitive and physical activities and to improve cardio-vascular health.  

Furthermore, the entire food system (including production and marketing) should be revised and changed: the goal is to stimulate the consumption of natural and nutritious foods and to reduce the consumption of sugary and ultra-processed foods.

Public health programs should be offered to the general population (with special attention to high-risk groups), including:

  • hypertension and diabetes treatment in midlife
  • prevention of head injury through traffic awareness campaigns and use of safety equipment at work and sports
  • support smoking cessation
  • reduce air pollution, promoting use of bicycles and public transport. Reduce second-hand tobacco smoke exposure.
  • encourage use of hearing aids for hearing loss and reduce hearing loss by protection of ears from excessive noise exposure
  • provide all children with primary and secondary education
  • support treatment and prevention of depression
  • limit alcohol intake.

At individual level, a healthy lifestyle including a balanced diet, regular physical activity, social and intellectual activities throughout life and prioritizing contact with nature should be sought. 

Conclusion: At this point the project “Knowledge stops Dementia” can help by keeping you up to date on what is known and new about dementia prevention and treatment! On our webpage you find an increasing amount of information covering the topics above, hopefully supporting you in the implementation of personal measures for prevention and recovering.

We are happy to support you in living a healthy life and minimising your personal risk of dementia. At the same time, we also offer support for your loved ones who are already suffering from some form of dementia. Don’t forget to register for our newsfeed! Not only you but also your children and grandchildren can only win!

Photo by Deva Darshan on Unsplash


Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020;396(10248):413-446.

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A study published in The American Journal of Medicine 2018, has demonstrated that maintaining a healthy diet in midlife is independently associated with a larger hippocampus years later and may protect against cognitive decline. The hippocampus is a structure located in the temporal lobe of each brain hemisphere and is directly involved in the process of memory. The volume of the hippocampus can be determined by brain magnetic resonance imaging (MRI). Decreasing of its volume is related to cognitive impairment and is used in clinical practice for the diagnosis of Alzheimer’s disease (hippocampus atrophy).

MRI Brain Diet

In this study, the quality of the diet of 459 participants (average age at baseline = 49 years) was assessed with a food-frequency questionnaire, which was administered in 1991-1993 and 11 years later, in 2002-2004. At the end of the follow up, around 13 years after the first questionnaire, participants underwent brain MRI with study of the hippocampus. Long-term healthy diet (showed by higher cumulative score on the Alternative Healthy Eating Index), was associated with a larger total hippocampus volume. This association was independent of sociodemographic factors, smoking habits, physical activity, cardiometabolic factors, cognitive impairment, and depressive symptoms and was more pronounced in the left hippocampus than in the right hippocampus.

A healthy diet, based on recommendations in the Alternative Healthy Eating Index 2010 (AHEI-2010) score is rich in vegetables, fruits, whole grains, nuts, legumes, omega-3 fats, and polyunsaturated fatty acids, and is light on sugar-sweetened drinks, red and processed meat, trans fat, and sodium-rich products. It is also characterized by low alcohol intake. 

The findings of this study support the hypothesis that overall diet may affect brain structures with a specific impact on hippocampus volume. 

Some other studies have demonstrated the influence of diet in brain structures. In most of these studies, diet quality was assessed by Mediterranean diet score, and higher scores (healthier diet) were found to be associated with larger cortical thickness, lower white matter hyperintensity burden, and preserved white matter microstructure. All these findings indicate better preservation of normal brain structure. 

Another previous study, published in 2015 in the BMC Medicine, had already shown that higher intakes of unhealthy foods, normally present in the Western diet, were independently associated with smaller hippocampal volume. This finding was originally observed on experimental animal models and suggested that a high-energy diet rich in saturated fats and refined sugars adversely affect neuronal plasticity and function. Animals maintained on a high-energy diet rich in fat and sugar showed lower performances in hippocampus-dependent spatial learning, object recognition, reduced hippocampus levels of brain-derived neurotrophic factor (BDNF) and impaired in blood-brain barrier integrity.

Accounting for the importance of hippocampus with long-term, declarative, episodic memory, as well as for flexible cognition network, this study reaffirms the need to recognize diet and nutrition as potential determinants of cognition, mental health and social behavior.


A Long-term healthy diet (and not various episodic restrictive diets) is the key to promote brain health and prevent dementia.

Thus, routine dietary counseling as part of a doctor’s office visit is very important at a patient’s level, but it should also be a high-priority public health goal.

To know more:

  1. Akbaraly, T et al. Association of Long-Term Diet Quality with Hippocampal Volume: Longitudinal Cohort Study. The American Journal of Medicine 2018
  2. Gu Y, Brickman AM, Stern Y, et al. Mediterranean diet and brain structure in a multiethnic elderly cohort. Neurology 2015;85 (20):1744–1751.
  3. Mosconi L, Murray J, Tsui WH, et al. Mediterranean diet and magnetic resonance imaging-assessed brain atrophy in cognitively normal individuals at risk for Alzheimer’s disease. J Prev Alzheimers Dis. 2014;1(1):23–32.
  4. Staubo SC, Aakre JA, Vemuri P, et al. Mediterranean diet, micronutrients and macronutrients, and MRI measures of cortical thickness. Alzheimers Dement. 2017;13(2):168-177.
  5. Jacka, F.N, Cherbuin, N, Anstey, KJ et al. Western diet is associated with a smaller hippocampus:a longitudinal investigation. BMJ 2015; 13:215
  6. Stranahan AM, Norman ED, Lee K, et al. Diet-induced insulin resistance impairs hippocampal synaptic plasticity and cognition in middleaged rats. Hippocampus. 2008;18(11):1085–1088.

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The negative effects of trans fats (also known as trans fatty acids, TFA) on our cardiovascular health have been known for a long time, they are among the most unhealthy food components of all.

In recent years, there has been an increase in the number of studies that prove an association between trans fat and  AD, as already reported by AMM in 2015 ( 1,628 healthy Japanese seniors were followed by a current study from Japan over a period of 10 years. In this context, the researchers examined TFA elaidic acid in the blood as a marker substance, which allows direct conclusions about the total TFA intake. 377 participants developed dementia, of which 247 developed Alzheimer’s and 102 vascular dementia.  Higher serum elaidic acid levels were significantly associated with a greater risk of developing Alzheimer’s disease, vascular dementia and total dementia. Patients whose blood trans fatty acid levels were in the higher range were 90% more likely to develop Alzheimer’s disease. These relationships remained significant even after adjustment for nutritional factors, including total energy intake and the intake of saturated and polyunsaturated fatty acids.

Current situation in Germany

In the Japanese study, the TFA was consumed with sweet baked goods, crackers, ice cream and such, but what is the current exposure situation in Germany?

TFA can get into food in different ways:

  •  produced by bacterias in the rumen of ruminants (such as cows, sheep and goats) and thus enter muscle meat and milk. A health-promoting effect is even being discussed concerning these ruminant TFA.
  • industrially produced when processing vegetable oils, the so-called partial hydrogenating process. These TFA have been used extensively in industrial food production.
  • while frying and deep-frying processes, whereby the TSF are almost completely transferred from the fat into the fried food.

In 2016, the EU Commission published a draft law to limit trans fats in foods, according to which the content of industrial TSAs is to be limited to 2% in the total fat from 2021. National regulations exist only in individual member states (e.g. Denmark, Finland) and in Switzerland. The WHO has also launched a global initiative with the ‘REPLACE’ programme, which aims to eliminate it (to 1% of total calories) worldwide by 2023.

The good news is that although there is still no mandatory national regulation in Germany, fortunately, industrial TFA are virtually no longer used in pre-packaged foods. They have been almost completely replaced by palm oil or palm kernel oil, which is at least better for health, but unfortunately causes different kinds of problems. Problems with regard to TFA contents of more than 2% in total fat are posed by unpackaged, bulk or industrially-like prepared foods sold in snack bars and bakery chains, as no list of ingredients is required by law, and single cases with extremely high TFA contents are still being identified.

Risk of TFA formation by radicals in the body

Biological membranes, which occur in every cell of the body, consist of a double layer of phospholipids. They contain a high proportion of fatty acids, whereby their content of unsaturated (non-trans) fatty acids positively influences the properties of these cell membranes. Therefore, the formation of TFA in the membranes poses an apparently great danger: As soon as the fatty acids within the membranes are converted to the trans configuration and thus, TFA are generated, this can have a negative effect on the fluidity of the membrane and promote the development of chronic diseases.

A few years ago, a study showed that rats fed TFA-free food for lifetime had implemented trans-isomers of mono- and polyunsaturated fatty acids (oleic, linoleic, linolenic and arachidonic acid) in liver, kidneys, heart, adipose tissue and erythrocytes. Thus, it was proven that TFAs can be formed in the organism even if the food does not contain any TFAs. Subsequent studies have also shown that free radicals are responsible for the formation of TFAs in the body. Free radicals can be produced in the organism during essential metabolic processes under physiological conditions, but also by external influences such as cigarette smoke, air pollution, organic solvents or irradiation. Due to their high chemical reactivity, these free radicals can cause oxidative damage to cellular macromolecules. In addition, the increased occurrence of TFAs formed in the body, especially of trans arachidonic acid, has been observed due to accumulated radical stress in various pathological states, such as inflammation, diabetes and Alzheimer’s disease.

This became very obvious when a study using an Alzheimer’s animal model revealed that TFAs were found only in the brain and hippocampus of mice carrying a gene specific for Alzheimer’s disease, but not in healthy animals. This result suggests that stress due to amyloid β-mediated radicals that accumulated during the development of Alzheimer’s disease causes cis-trans isomerisation of fatty acids in neurons of Alzheimer’s mice. In a subsequent study, it was further shown that the animals had significantly reduced levels of TFA in the brain and hippocampus after administration of two antioxidant substances for 3 months. These studies thus imply that the administration of antioxidant substances may be a possible strategy to prevent the body’s own formation of TFA during the development of chronic diseases such as Alzheimer’s disease. Based on the results of all intervention studies, a variety of antioxidant vitamins and polyphenolic compounds derived from plants, including curcumin and resveratrol, appear to inhibit TFA formation in the body (Figure 1, modified after Hung et al. 2016).

Inhibition Trans Fatty Acids
Figure 1: Potential Inhibition of the Formation of Trans Fatty Acids in Human Membranes by Dietary Antioxidants

The connection between Alzheimer’s disease and the consumption of trans-fatty acids (TFA) is becoming increasingly evident, although the exposure to TFA through pre-packaged food to TFA in Germany has decreased in recent years. The industry has reacted to the EU’s legal regulation, which will come into force in 2021, of a maximum of 2% of total fat. However, when you visit the snack bar and the bakery chain, remember that trans fats may still play a not inconsiderable role here.

However, the real danger of TFA seems to be in the body, as they can be produced there by free radicals. But you can do something about it with a healthy diet: Ensure your supply of antioxidant micronutrients from food and, if necessary, supplements, before the TFA otherwise formed in your body damage your cell membranes and drive you insane!


  1. Honda,T et al (2019) Serum elaidic acid concentration and risk of dementia: The Hisayama Study. Neurology, 2019
  2. Informationsblatt der Europäischen Union 2019
  3. Bähr M, Jahreis G, Kuhnt K (2011) Trans fatty acids in foods on the German market and in human tissue. Ernährungsumschau 9
  4. Ghebreyesus T, Frieden TR (2018) REPLACE: a roadmap to make the world trans fat free by 2023. The Lancet 391
  5. Messdaten zu Trans-Fettsäuren aus der amtlichen Überwachung zu insgesamt 2.633 Proben aus den Jahren 2014-2017, Auskunft des Bundesamts für Verbraucherschutz und Lebensmittelsicherheit (BVL) vom 31. März 2017
  6. Kuhnt K, Degen C, Jahreis G (2015) Evaluation of the Impact of Ruminant trans Fatty Acids on Human Health: Important Aspects to Consider. Crit Rev Food Sci Nutr. 56
  7. Hung, WL et al (2016) Endogenous formation of trans fatty acids: Health implications and potential dietary intervention, Journal of Functional Foods 25

Photo by Khairul Onggon on Pexels

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Red wine drinkers are generally good-natured people and known for mastering life with pleasure and relaxation. These alone are two protective factors against dementia, because stress is poison for the brain (but more about this later on). In addition, a secondary plant substance present particularly in red wine is increasingly attracting the interest of research and prevention in Alzheimer’s disease: resveratrol.

Resveratrol has numerous biological and pharmacological protective effects and became well-known back in the mid-1990s in connection with the ‘French Paradox’. It stands for the observation that French people live longer than Germans and Americans despite their supposedly unhealthier lifestyle, especially because of their higher alcohol consumption, and that the frequency of heart attacks in France is three times lower than in the USA. In the following years, resveratrol became the focus of research and showed anti-inflammatory, antioxidant, cancer-inhibiting, heart protecting and life-prolonging properties in numerous test models both in vitro and in vivo and was considered a new miracle cure.

Resveratrol and Alzheimer

The first indications that resveratrol could also be responsible for the protective effect of red wine in Alzheimer patients were shown by epidemiological studies conducted by a French research group in 1997, which showed an inverse correlation between moderate wine consumption and the occurrence of Alzheimer’s disease: in the group of moderate wine drinkers (250 – 500 ml per day) the risk of dementia was reduced by a factor of 5.

It showed that resveratrol not only unfolds its positive effects in a single way, but also has a multi-mechanistic effect. It has a beneficial effect on various processes, all of which play a decisive role in the development of Alzheimer’s disease:

  1. reduction of amyloid plaques 
  2. reduction of neurofibrillary tangles 
  3. regulatory role in autophagy processes 
  4. anti-inflammatory effect 
  5. antioxidant effects

Detailed explanations on these topics can be found on the page: Resveratrol

Clinical studies

Based on these convincing results, the therapeutic potential of resveratrol in Alzheimer’s patients is currently being tested in clinical trials. Two recent pilot studies have shown that resveratrol can easily cross the blood-brain barrier in humans and penetrate brain tissue – as it has been detected in cerebrospinal fluid. Resveratrol was well tolerated by all volunteers and had no side effects up to a dose of 5 grams per day. Both double-blind studies show evidence of positive effects of resveratrol in humans. 

In addition, resveratrol is already part of the multifactorial approach of the American neurologist Dale Bredesen, who, with his therapy known as ‘ReCode’ (Reversal of Cognitive Decline), has managed to clinically reverse Alzheimer’s courses in early stages (see also the interview with Dr. Bredesen in the media library).

Whether fed with a glass of red wine in the evening or by other non-alcoholic means – but preferably from natural sources – the secondary plant substance resveratrol appears to be responsible for protective effects in the development of dementia due to its diverse mechanisms of action. It could therefore be a promising preventive and possibly therapeutic approach in the fight against Alzheimer’s disease.

In this sense: treat yourself to a glass of red wine or grape juice in the evening and enjoy life. Your grey cells will be grateful!

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This descriptive documentation of the Arte TV channel shows very clearly the connections between an unbalanced diet, the resulting micronutrient deficiencies and the effects on the brain. Various experiments have shown that mice that grow up with a deficiency of omega-3 fatty acids have deficits in the formation of their neurons and are much more anxious.

A particularly striking example showed an experiment with field hamsters. Here a simple vitamin B3 deficiency was sufficient to trigger aggressive behaviour during mating in over 80% of females. In the further course of the experiment, these females even ate their offspring directly after birth. After the vitamin B3 deficiency had been remedied, the females showed normal behaviour again, despite continued unbalanced diet  (thus the vitamin B3 factor could be clearly identified as the trigger).

In humans, long-term observations and studies showed similar results. Already in the uterus, the nutrition of the mother decides about the brain development and the emotional development of the fetus and newborn.

Mothers who eat “junk food” with a low omega-3 fatty acid concentration and high sugar content give birth to children that tend to act more aggressive. If this form of nutrition is continued in childhood, aggressive  behaviour, anxiety and attention disorders are pre-programmed. If there is a lack of omega-3 fatty acids, the function of the brain is disturbed, the communication between neurons and the neurogenesis are impaired.

The second cardinal error of Western nutrition is the flooding of highly processed foods with cheap refined sugars. Experiments have shown that this hidden sugar poisoning may show higher addiction effects  than cocaine. The consequences are insulin resistance, diabetes and dementia.

Of course, this form of unbalanced nutrition also has an effect on the intestines and the gut microbiota (and their genetic diversity, the microbiome), which have a significant influence on the health of our body and mind. Concrete examples show that the density of nutrients in food influences the way we   make decisions and solve daily problems. But we do not want to reveal too much here, watch for yourself:


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Unfortunately this excellent video don’t provide English subtitles, a more scientific alternative about the MIND diet in English can be found here:


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As far as mental and brain health is concerned, nutrition seems to be a major component of prevention, particularly with regard to dementia.  An alteration towards the Mediterranean diet or even better the MIND diet  increases our chances to remember the names of our grandchildren in the future and to actively participate in life. Just leave the “industrial garbage” on the shelf, even if it is sometimes difficult.

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Curcumin is a yellow pigment contained in turmeric (Curcuma longa). The benefits of curcumin in different organ systems have been extensively documented in the past in several neurological diseases and cancer. Curcumin has received worldwide recognition for its potent antioxidant, anti-inflammatory, anti-cancer and antimicrobial activities. Curcumin has been successfully used to treat diabetes and arthritis, as well as liver, kidney and cardiovascular diseases. Recently, attention has focused on the use of curcumin to prevent or delay the onset of neurodegenerative diseases. A recently published review study ( summarized the use of curcumin in different neurological diseases, including Alzheimer’s disease. Recent advances in curcumin formulations and strategies to overcome low bioavailability are discussed as well as toxicity and ongoing clinical trials.


There is good evidence that turmeric consumption has various potential health benefits not only for older people. In addition to its role in treatment and prevention, curcumin acts in AD therapies as an antioxidant, anti-inflammatory, inhibitor of Aβ aggregation and chelator of metal ions. These effects are, regardless of the results of clinical studies, a good reason to include curcuminoids in our regular diet – e.g. in the form of strong curries.

Further information about the effect of curcumin on Alzheimer’s can be found at Curcumin and Alzheimer’s Dementia…


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