How Alcohol Affects Nutrition, Vitamin Levels, and Metabolism in the Human Body

My social connections are Sunday night, jazz; Tuesday night, jazz; Thursday night, trivia. All at bars so some alcohol is involved and since preventing dementia is vastly more important that this problem which doesn't exist for me.

My diet quality is pretty decent now with meals from Home Chef.

How Alcohol Affects Nutrition, Vitamin Levels, and Metabolism in the Human Body

By Hugo Francisco de SouzaReviewed by Benedette Cuffari, M.Sc.

Introduction
Alcohol and micronutrient absorption and status
Effects of alcohol on metabolic pathways
AUD and diet quality
Clinical and public health implications
Research gaps and future directions
Conclusions
References
Further reading

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Chronic alcohol consumption disrupts nutrient absorption, metabolism, and dietary quality, contributing to widespread micronutrient deficiencies and metabolic dysfunction. These nutritional disturbances exacerbate liver disease, neurological damage, and recovery challenges in individuals with alcohol use disorder.

 Image Credit: Valentyn Volkov / Shutterstock.com

Introduction

This article explores the intersection between drinking and nutrition to reveal how alcohol-induced malnutrition can perpetuate a cycle of craving and relapse.

Alcohol use disorder (AUD) is strongly associated with disturbances in nutritional status arising from both reduced dietary intake and alcohol-mediated disruptions in nutrient absorption, metabolism, storage, and utilization. These disturbances contribute to systemic complications, including liver disease, neurological dysfunction, immune impairment, and metabolic dysregulation. Alcohol-derived calories frequently displace nutrient-dense foods, while chronic exposure alters gastrointestinal, hepatic, and endocrine processes required for maintaining nutritional homeostasis.1,3,4

Alcohol and micronutrient absorption and status

The most severe nutritional consequence of chronic alcohol consumption is the depletion of micronutrients that occurs due to impaired intestinal absorption and increased renal excretion.1 Specifically, ethanol acts as a molecular disruptor of the brush border membrane (BBM) by targeting specific transporters required for the uptake of water-soluble vitamins.

Chronic ethanol consumption has been directly implicated in vitamin B1 deficiency by inhibiting the activity of SLC19A2, a transporter protein for thiamine. Similar inhibitory effects on the absorption of vitamins C and B12, riboflavin, biotin, and folate have been clinically observed.

Alcohol can also impair sodium-dependent and carrier-mediated nutrient transport systems located on intestinal epithelial cells, including transporters involved in glucose, amino acid, and micronutrient uptake. Disruption of these brush-border transport processes alters the function of intestinal enterocytes and contributes to malabsorption of essential nutrients in the small intestine.2

Alcohol consumption also alters the absorption and systemic concentrations of several macroelements and trace elements, including magnesium, potassium, sodium, calcium, selenium, zinc, chromium, and phosphorus. These disturbances may result from gastrointestinal malabsorption, increased urinary losses caused by alcohol’s diuretic effects, and impaired hepatic storage or metabolic regulation.7

Ethanol intake also reduces intestinal absorption of calcium, zinc, iron, and magnesium, in addition to interfering with dietary fat absorption in a dose-dependent manner. Drinking alcohol, even in moderate amounts, also reduces glucose absorption by reducing its maximal rate of uptake to limit its active transport into the bloodstream, rather than through its interactions with a specific transporter.

In addition to water-soluble vitamins, chronic alcohol use may also contribute to deficiencies in fat-soluble vitamins (A, D, E, and K), particularly in individuals with liver disease, steatorrhea, or impaired lipid digestion. These vitamins play essential roles in immune function, bone metabolism, antioxidant defense, and blood coagulation, and their depletion may exacerbate complications associated with chronic alcohol use.6

Ethanol possesses a high caloric density despite being entirely devoid of essential vitamins, minerals, and macronutrients.1 Thus, in addition to the direct effects of ethanol intake on nutrient absorption, primary malnutrition also arises due to the substitution of dietary carbohydrate, protein, and fat intake with alcoholic calories.

Furthermore, alcohol consumption can disrupt iron homeostasis through alterations in the hepatic hormone hepcidin, which regulates intestinal iron absorption and systemic iron distribution. Experimental evidence suggests that alcohol exposure can suppress hepatic hepcidin expression while modifying ferroportin activity and other iron-regulatory proteins.  These alterations may lead to abnormal iron distribution and contribute to oxidative stress and liver injury in alcohol-related liver disease.8

The nutritional deficiencies observed in individuals with alcohol use disorder (AUD) contribute not only to physiological impairments such as alcohol-related liver disease but also to the core symptoms of alcoholism, such as cognitive dysfunction and increased negative affect, thereby contributing to the vicious cycle of alcoholism and comorbidity.1”

Effects of alcohol on metabolic pathways

Hepatic ethanol metabolism primarily occurs through the alcohol dehydrogenase (ADH) pathway, which generates acetaldehyde, a highly reactive toxin that forms DNA and protein adducts.1 This process further reduces nicotinamide adenine dinucleotide (NAD+) to NADH, which significantly increases the NADH/NAD+ ratio. The subsequent inhibition of fatty acid oxidation while promoting triglyceride synthesis directly leads to hepatic steatosis.2

Additional metabolic pathways involved in ethanol metabolism include the microsomal ethanol-oxidizing system (MEOS), largely mediated by cytochrome P450 2E1 (CYP2E1), and catalase-mediated oxidation in peroxisomes. Activation of these pathways promotes the generation of reactive oxygen species (ROS), contributing to oxidative stress, lipid peroxidation, mitochondrial dysfunction, and inflammatory signaling.7

Ethanol also acts as a metabolic toxin by inhibiting the mammalian target of rapamycin (mTOR) pathway, a central regulator of muscle protein synthesis. Furthermore, alcohol reduces the phosphorylation of downstream targets such as ribosomal protein S6 kinase beta-1 (S6K1) and eukaryotic translation initiation factor 4E-binding protein 4EBP1, thereby preventing protein synthesis.4

These alterations contribute to skeletal muscle wasting, metabolic dysfunction, and impaired energy homeostasis.9 Chronic inflammation and oxidative stress further suppress anabolic signaling pathways involved in tissue repair and metabolic regulation.7,9

AUD and diet quality

Diet quality in individuals with AUD can vary greatly during periods of active use and post-cessation recovery. During active drinking, diet quality is generally poor, with patients scoring an average of 42.9 on the Healthy Eating Index-2015 (HEI-2015), compared with 54.3 in healthy controls.4 Using the Nova classification system, ultra-processed foods accounted for approximately 51.8% of total energy intake among individuals with active AUD.4

Despite apparently adequate caloric intake in some individuals with AUD, micronutrient deficiencies remain common because alcohol interferes with nutrient absorption, metabolism, and biological utilization.4

How i-REBOUND gave stroke survivors everywhere access to online diet and exercise rehab tools

 In case you need something like this because your incompetent? doctor failed you!

How i-REBOUND gave stroke survivors everywhere access to online diet and exercise rehab tools

Background

A world-first website featuring evidence-based resources to help people living with stroke move more and eat well to reduce the risk of a second stroke has reached 25,000 people since its launch on 7 November 2022. i-REBOUND connects survivors of stroke to fit-for-purpose resources via the internet.The project was developed to meet the diet and exercise support gap that stroke survivors reported after they were discharged from hospital.It also helps meet the needs of people in regional and rural areas where allied health support can be hard to access. This is a critical factor because regional and rural Australians are 17% more likely to have a stroke than their metropolitan counterparts.

The Challenge

Regional and rurally-located people living with stroke don’t have access to allied health support services. No easily accessible, online supports designed for and by stroke survivors. Increased risk of secondary stroke if post-stroke exercise and diet guidelines aren’t met

The Solution

i-REBOUND lead, University of Newcastle researcher Professor Coralie English from the Heart and Stroke Research Program, says, “We know that poor diet and inactivity are strong risk factors for stroke and recurrent stroke but there was no support for people when they left hospital. We wanted to change that,” says Professor English.The i-REBOUND website, funded by The Nancy and Vic Allen Stroke Prevention Memorial Grant took 18 months to develop, and was created in close partnership and consultation with stroke survivors. The people in the videos on the site are stroke survivors and the hints and tips they deliver are rooted in lived experience.

Impact

Stroke survivor Brian Beh says,“As a stroke survivor, i-REBOUND is an excellent example of the power of collaboration across the broad vista of the stroke landscape. “i-REBOUND provides relevant information on several key elements in after stroke living – dietary tips, exercise routines and insights into the personal and social challenges that are encountered by survivors living with stroke. “The success of i-REBOUND was underpinned by the sage and strategic leadership of Coralie English, who led a group of bolschy, committed, and opinionated stroke survivors, stroke researchers, and clinicians. “The messages on the i-REBOUND website feature actual stroke survivors, in an often brutally honest manner – that is why I use it. stroke survivors can see themselves when they visit the site,” The i-REBOUND website has 23,946 users in 102 countries and features 175+ recipes, exercises, and resources tailored for stroke survivors.

Next Steps

Professor English and her team are hoping to progress the program.

She says, “We are really needing another injection of funds to help us take it to next level of structured, modulised education /self-management product, and to find sustainable ways to refresh content going forward. We are part of bid lead by HMRI to work on developing it into a more comprehensive secondary prevention platform.”

 Check out the i-REBOUND website here.

Professor English and her team are hoping to progress the program. She says, “We are really needing another injection of funds to help us take it to next level of structured, modulised education /self-management product, and to find sustainable ways to refresh content going forward. We are part of bid lead by HMRI to work on developing it into a more comprehensive secondary prevention platform.” Check out the i-REBOUND website here

Eggs May Not Be Bad for Your Heart After All

Didn't this research already answer the question? And what the hell are fortified eggs?

Fortified eggs have a high level of nutrients because specific components are added to hens' feed. Good luck finding those.

Association of egg intake with blood lipids, cardiovascular disease, and mortality in 177,000 people in 50 countries April 2020

With this line: According to the findings, no significant links exist between egg consumption and blood lipids, mortality, or major CVD events in this analysis of 3 large international prospective investigations involving approximately 177,000 people, 12,701 deaths, and 13,658 CVD events from 50 countries in 6 continents.

The latest here:

 

Eggs May Not Be Bad for Your Heart After All

Subgroup analyses signal a possible benefit among older adults and those with diabetes

Mar 28, 2024

Contact: Nicole Napoli, nnapoli@acc.org, 202-669-1465

WASHINGTON (Mar 28, 2024) -

Whether you like your eggs sunny-side up, hard boiled or scrambled, many hesitate to eat them amid concerns that eggs may raise cholesterol levels and be bad for heart health. However, results from a prospective, controlled trial presented at the American College of Cardiology’s Annual Scientific Session show that over a four-month period cholesterol levels were similar among people who ate fortified eggs most days of the week compared with those who didn’t eat eggs.

A total of 140 patients with or at high risk for cardiovascular disease were enrolled in the PROSPERITY trial, which aimed to assess the effects of eating 12 or more fortified eggs a week versus a non-egg diet (consuming less than two eggs a week) on HDL- and LDL-cholesterol, as well as other key markers of cardiovascular health over a four-month study period.

“We know that cardiovascular disease is, to some extent, mediated through risk factors like high blood pressure, high cholesterol and increased BMI and diabetes. Dietary patterns and habits can have a notable influence on these and there’s been a lot of conflicting information about whether or not eggs are safe to eat, especially for people who have or are at risk for heart disease,” said Nina Nouhravesh, MD, a research fellow at the Duke Clinical Research Institute in Durham, North Carolina, and the study’s lead author. “This is a small study, but it gives us reassurance that eating fortified eggs is OK with regard to lipid effects over four months, even among a more high-risk population.”

Eggs are a common and relatively inexpensive source of protein and dietary cholesterol. Nouhravesh and her team wanted to look specifically at fortified eggs as they contain less saturated fat and additional vitamins and minerals, such as iodine, vitamin D, selenium, vitamin B2, 5 and 12, and omega-3 fatty acids.

For this study, patients were randomly assigned to eat 12 fortified eggs a week (cooked in whatever manner they chose) or to eat fewer than two eggs of any kind (fortified or not) per week.  All patients were 50 years of age or older (the average age was 66 years), half were female and 27% were Black. All patients had experienced one prior cardiovascular event or had two cardiovascular risk factors, such as high blood pressure, high cholesterol, increased BMI or diabetes. The co-primary endpoint was LDL and HDL cholesterol at four months. Secondary endpoints included lipid, cardiometabolic and inflammatory biomarkers and levels of vitamin and minerals. 

Patients had in-person clinic visits at the start of the study and visits at one and four months to take vital signs and have bloodwork done. Phone check-ins occurred at two and three months and patients in the fortified egg group were asked about their weekly egg consumption. Those with low adherence were provided additional education materials.

Results showed a -0.64 mg/dL and a -3.14 mg/dL reduction in HDL-cholesterol (“good” cholesterol) and LDL cholesterol (“bad” cholesterol), respectively, in the fortified egg group. While these differences weren’t statistically significant, the researchers said the differences suggest that eating 12 fortified eggs each week had no adverse effect on blood cholesterol. In terms of secondary endpoints, researchers observed a numerical reduction in total cholesterol, LDL particle number, another lipid biomarker called apoB, high-sensitivity troponin (a marker of heart damage), and insulin resistance scores in the fortified egg group, while vitamin B increased.

“While this is a neutral study, we did not observe adverse effects on biomarkers of cardiovascular health and there were signals of potential benefits of eating fortified eggs that warrant further investigation in larger studies as they are more hypothesis generating here,” Nouhravesh said, explaining that subgroup analyses revealed numerical increases in HDL cholesterol and reductions in LDL cholesterol in patients 65 years or older and those with diabetes in the fortified egg group compared with those eating fewer than two eggs.

So why have eggs gotten a bad rap? Some of the confusion stems from the fact that egg yolks contain cholesterol. Experts said a more important consideration, especially in the context of these findings, might be what people are eating alongside their eggs, such as buttered toast, bacon and other processed meats, which are not heart healthy choices. As always, Nouhravesh said it’s a good idea for people with heart disease to talk with their doctor about a heart healthy diet.(Why? Your doctor knows nothing about diet!)

This single-center study is limited by its small size and reliance on patients’ self-reporting of their egg consumption and other dietary patterns. It was also an unblinded study, which means patients knew what study group they were in, which can influence their health behaviors.

The study was funded by Eggland’s Best.

Nouhravesh will present the study, “Prospective Evaluation of Fortified Eggs Related to Improvement in the Biomarker Profile for Your Health: Primary Results from the PROSPERITY Trial,” on Saturday, April 6, 2024, at 12:45 p.m. ET / 16:45 UTC in Hall B4-5.

ACC.24 will take place April 6-8, 2024, in Atlanta, bringing together cardiologists and cardiovascular specialists from around the world to share the newest discoveries in treatment and prevention. Follow @ACCinTouch, @ACCMediaCenter and #ACC24 for the latest news from the meeting.

The Secret to Aging Gracefully? Simple Dietary Changes, Not Just Cutting Calories

Ask your doctor how this can be applied to humans.

The Secret to Aging Gracefully? Simple Dietary Changes, Not Just Cutting Calories

Summary: A simple dietary change, without caloric restriction, can promote healthier aging. The study in yeast cells revealed that a shift from a glucose-rich to a galactose-based diet led to molecular changes that typically accompany aging.

These findings challenge the long-held notion that only caloric restriction can lead to healthier, longer lives. While the study was conducted in yeast cells, known to share many cellular mechanisms with humans, further research is needed to explore the real-world implications.

Key Facts:

1. A dietary change from glucose to galactose reduced signs of aging in yeast cells, without needing caloric restriction.
2. The health benefits of caloric restriction disappear in mice when a normal diet is resumed, making alternative approaches necessary for longevity.
3. The positive effects were most pronounced when dietary changes were implemented in yeast cells at a young age, emphasizing the potential importance of early-life dietary choices.

Source: Babraham Institute

Researchers at the Babraham Institute are proposing an alternative link between diet and aging based on studies in yeast.

Dr Jon Houseley and his team have published their experiments, showing that healthy aging is achievable through dietary change without restriction by potentially optimising diet, and that ill-health is not an inevitable part of the aging process.

Scientists have long known that caloric restriction – intentionally consuming far less calories than normal without becoming malnourished – improves health in later life and may even extend life.

This avenue of research in yeast helps us to seek a more achievable way to improve healthy ageing though diet compared to sustained and severe calorie restriction, although more research is needed. Credit: Neuroscience News

However, studies in mice show that caloric restriction really needs to be maintained throughout life to achieve this impact, and the health benefits disappear when a normal diet is resumed.

Dr Houseley’s new research conducted in yeast suggests an alternative to calorie restriction can lead to improved health through the lifecycle.

“We show that diet in early life can switch yeast onto a healthier trajectory. By giving yeast a different diet without restricting calories we were able to suppress senescence, when cells no longer divide, and loss of fitness in aged cells.” Said Dr Dorottya Horkai, lead researcher on the study.

Rather than growing yeast on their usual glucose-rich diet, the researchers swapped their diet to galactose and observed that many molecular changes which normally accompany aging did not occur.

The cells grown on galactose remained just as fit as young cells even late in life, despite not living any longer, showing that the period of ill-health towards the end of life was dramatically reduced.

“Crucially, the dietary change only works when cells are young, and actually diet makes little difference in old yeast. It is hard to translate what youth means between yeast and humans, but all these studies point to the same trend – to live a long and healthy life, a healthy diet from an early age makes a difference.” explains Dr Houseley.

Yeast are good model organisms for studying aging as they share many of the same cellular machinery as animals and humans. This avenue of research in yeast helps us to seek a more achievable way to improve healthy aging though diet compared to sustained and severe calorie restriction, although more research is needed.

About this diet and aging research news

Author: Honor Pollard
Source: Babraham Institute
Contact: Honor Pollard – Babraham Institute
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Senescence in yeast is associated with amplified linear fragments of chromosome XII rather than ribosomal DNA circle accumulation” by Jon Houseley et al. PLOS Biology

Unlocking the fountain of youth: Diet and exercise have a remarkable impact on cognition in older adults

Still pretty useless, just guidelines; NOT EXACT PROTOCOLS.

Unlocking the fountain of youth: Diet and exercise have a remarkable impact on cognition in older adults

By Neha MathurJun 13 2023Reviewed by Benedette Cuffari, M.Sc.

Given the vast number of people in the United States who are approaching 65 years of age, there is a need for interdisciplinary research on factors influencing the trajectory of cognition and brain aging in older adults. In a recent review published in Nutrients, researchers examine the collective effect of diet and exercise interventions on age-related cognition and brain health changes. 

Study: Impact of Diet and Exercise Interventions on Cognition and Brain Health in Older Adults: A Narrative Review. Image Credit: Isarat / Shutterstock.com

Age-related cognitive decline

Reduced processing speed is one of the major cognitive deficits observed in older adults, in addition to impaired semantic and episodic memory. Likewise, working memory that actively maintains information in the short term to enable goal-directed decision-making also declines because of aging.

Reduced working memory results in a corresponding reduction in executive functions in advanced age. Due to structural and functional changes in the brain, aging also affects an individual's crystallized and fluid intelligence.

Structural changes in the brain associated with aging include reduced gray matter volume and cortical thickness. Gray matter volume, a measure of neuronal and glial cell bodies, declines in volume within multiple brain regions, including the medial temporal lobe of the hippocampus and entorhinal cortex during aging. Specifically, age-related reduction of hippocampal volume, resulting from neuronal cell loss and a decrease in neurogenesis, is associated with decreased cognitive performance on memory, spatial learning, and emotional regulation tasks. 

Effect of diet and exercise on aging 

It is crucial to understand the relationship between nutrient consumption and neuronal function, neurometabolic processes, and cognitive decline. 

There is growing evidence that nutrients from various foods across multiple food groups have synergistic effects beyond the effects of individual nutrients. For example, the absorption of vitamins from green salad improves when served with olive oil and vinegar rather than a fat-free ranch dressing. 

Food Adulteration in the Honey Industry eBook Learn how to test and ensure honey authenticity throughout the supply chain with this free eBook. Download the latest edition

To date, the Mediterranean diet (MeDi), Dietary Approaches to Stop Hypertension (DASH), and Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diets are most frequently referenced in the literature. Each of these diets appears to improve neurological signs of aging, including cell membrane and vascular integrity, inflammation, resolution, and oxidation, as well as lipid and glucose metabolism.

Considerable evidence suggests that the MeDi and MIND diets are associated with both general and domain-specific facets of cognitive ability. For example, several studies have associated the MeDi diet with attention and long-term memory. Likewise, adherence to the MIND diet is positively associated with visuospatial ability, perceptual speed, and executive function.

The impact of the ketogenic diet (KD) and intermittent fasting (IF) on cognition and brain function have also been widely studied, as weight management diets appear to improve cognitive functioning. Likewise, weight loss achieved through bariatric surgery enhances attention, memory, and executive function.

In addition to diet, exercise positively affects cognition, as demonstrated by a previous study in which overweight and obese adults were enrolled in a one-year behavioral weight loss intervention. These patients were on an energy-restricted diet, an energy-restricted diet with 150 minutes of moderate-intensity exercise every week, or an energy-restricted diet with 250 minutes of exercise every week. 

Post-intervention, weight markedly decreased across both groups. More specifically, the high-exercise group improved their performance on Iowa Gambling Task (IGT) reward relative to the other two study groups. Overall, more exercise with behavioral weight loss regimens had an additional benefit on executive functioning, even with no weight loss benefits.

Endurance exercise typically encompasses walking, jogging, running, swimming, and cycling, with walking being the most practiced form among older adults. Higher endurance fitness levels are associated with less age-related brain volume decline. 

Randomized controlled trials examining the role of endurance exercise on cognition have led to mixed results. However, all evidence suggests that endurance exercise in older adults improved cognitive performance, visual attention, and memory, promoted brain plasticity, and weakened hippocampal atrophy.

Similarly, a recent systematic review found that resistance training positively affected older adults' executive and global cognitive functions. This form of exercise also positively impacted memory, albeit weakly, and did not significantly improve attention. Additionally, tri-weekly, as compared to biweekly resistance training, positively affected general cognitive abilities.

No evidence of an interference effect of aerobic and resistance training has been reported. However, literature comparing resistance or combined exercise to a non-exercise control is limited. Thus, it remains unclear which exercises should be prescribed to maintain and enhance cognition and brain health among older adults.

Behavioral interventions like yoga appear to mitigate age-related and neurodegenerative decline. In one review examining the effects of practicing yoga on brain structures, function, and cerebral blood flow, yoga positively affected the structure and function of the hippocampus, prefrontal and cingulate cortex, amygdala, and neuronal networks. 

A recent literature review evaluating the effect of tai chi, a traditional Chinese martial art, on brain structure and neurobehavior changes found that this form of exercise also increased cortical grey matter volume, improved neural activity and homogeneity, and increased neural connectivity in the frontal, temporal, and occipital lobes, cerebellum, and thalamus.

Conclusions

All diets evaluated in this review addressed factors associated with aging and neurodegenerative diseases like Alzheimer's disease and related dementias (ADRD). Depending on the type and intensity, exercises were found to positively affect brain vascularization, neurotransmitter regulation, growth factors, and neurogenesis.

Journal reference:

• Key, M. N., & Szabo-Reed, A. N. (2023). Impact of Diet and Exercise Interventions on Cognition and Brain Health in Older Adults: A Narrative Review. Nutrients 15(11);2495. doi:10.3390/nu15112495

Does Diet Matter? Study Questions Links Between Diet and Dementia

 Am I reading this right? Diet has almost nothing to do with dementia?

You contradicted these?

Can Certain Foods Really Stave Off Dementia? April 2022 

Enjoy Meat? Diverse Side Dishes Lower Dementia Risk May 2020 

 

The latest here:

Does Diet Matter? Study Questions Links Between Diet and Dementia

Diet combined with other risk-reduction strategies may show different results

by Judy George, Deputy Managing Editor, MedPage Today October 12, 2022

Midlife dietary habits were not tied to dementia incidence over a 20-year period, a prospective study in Sweden showed.

Adhering to conventional dietary recommendations or to a modified Mediterranean diet was not linked with lower incidence of all-cause dementia, Alzheimer's disease dementia, vascular dementia, or amyloid pathology, reported Isabelle Glans, MD, of Lund University in Sweden, and colleagues.

"The study does not exclude a possible association between diet quality and subsequent development of dementia," they wrote in Neurology.

"However, the present Swedish dietary recommendations, which are in line with those in the U.K. and U.S., or according to the Mediterranean dietary pattern, could not be confirmed to be associated with prevention of dementia," the researchers added.

It's "critically important to better understand the links between diet and nutrition and dementia risk," observed Heather Snyder, PhD, vice president of medical and scientific relations at the Alzheimer's Association in Chicago, who wasn't involved with the study.

"To get there, the connections between diet and dementia risk must be examined in multiple studies across multiple populations and even multiple countries," Snyder told MedPage Today.

"These new results represent one study and should be considered in the bigger landscape of the ongoing work," she emphasized. "This is an observational study that can find an association between factors, but does not prove causation. For that, we need an intervention study. Fortunately, there are studies today that are testing dietary and nutrition-related interventions."

"Beyond that, existing data suggest that there is synergy between different risk-reduction strategies and these strategies should be considered in combination, not one at a time," Snyder pointed out. For example, the 2-year U.S. POINTER trial is evaluating whether lifestyle interventions that target multiple risk factors can benefit people with a higher risk of cognitive decline.

The Swedish study isn't the first to suggest diet and dementia are not related. "The findings are overall in line with previous long-term studies addressing this topic," noted Nils Peters, MD, of the University of Basel in Switzerland, and Benedetta Nacmias, PhD, of the University of Florence in Italy, in an accompanying editorial.

"Diet as a singular factor may not have a strong enough effect on cognition, but is more likely to be considered as one factor embedded with various others, the sum of which may influence the course of cognitive function (diet, regular exercise, vascular risk factor control, avoiding cigarette smoking, drinking alcohol in moderation, etc.)," they wrote. "Thus, diet should rather be regarded as one part of a multidomain intervention with respect to cognitive performance."

Glans and colleagues followed 28,025 people in the Swedish population-based Malmö Diet and Cancer Study who were dementia-free at baseline and who had baseline exams from 1991-1996. Mean baseline age was 58 and 61% were women.

The researchers used a 7-day food diary, a detailed food frequency questionnaire, and a 45-60 minute interview to evaluate dietary habits at baseline.

Swedish dietary guidelines scores, designed to reflect a healthy diet based on Swedish nutritional guidelines, were calculated based on average daily food intake. Eating patterns also were assessed by adherence to a modified Mediterranean diet that focused on a high intake of vegetables, legumes, fruits, fish, and healthy fats and a low intake of dairy products, meat, and saturated fatty acids.

Dementia diagnoses were determined by memory clinic physicians. A subpopulation of 738 participants had analyses of cerebrospinal fluid (CSF) levels of amyloid-beta 42 when they were referred to the Skåne University Hospital in Malmö memory clinic after developing clinical signs of cognitive impairment.

The primary outcome was progression to all-cause dementia. Secondary outcomes were progression to Alzheimer's dementia and vascular dementia. Over a median follow-up of 19.8 years, 1,943 people (6.9%) were diagnosed with all-cause dementia.

A comparison of worst-versus-best adherence to conventional dietary recommendations showed no difference in risk of all-cause dementia (HR 0.93, 95% CI 0.81-1.08), Alzheimer's dementia (HR 1.03, 0.85-1.23) or vascular dementia (HR 0.93, 95% 0.69-1.26).

Likewise, worst-versus-best adherence to a modified Mediterranean diet did not lower the risk of developing all-cause dementia (HR 0.93, 95% 0.75-1.15), Alzheimer's dementia (HR 0.90, 95% 0.68-1.19) or vascular dementia (HR 1.00, 95% 0.65-1.55).

In sensitivity analyses, results were similar when excluding people who developed dementia within 5 years or people with diabetes. Neither conventional diet recommendations nor a modified Mediterranean diet had a significant association with abnormal CSF amyloid-beta markers.

The results come with several caveats, Glans and colleagues noted. Dietary data were collected only at baseline and dietary habits may have changed during the follow-up period. In addition, participants with CSF samples were not randomized, but were recruited based on clinical indications.

"Randomized controlled trials are needed to provide additional evidence regarding the potential role of diet in relation to Alzheimer's disease pathology," they wrote.

• Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

The study was funded by the Swedish Research Council, the Knut and Alice Wallenberg Foundation, the Marianne and Marcus Wallenberg Foundation, the Strategic Research Area MultiPark at Lund University, the Swedish Alzheimer Foundation, the Swedish Brain Foundation, the Parkinson Foundation of Sweden, the Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse, the Skåne University Hospital Foundation, Regionalt Forskningsstöd, and the Swedish federal government.

Glans dislcosed no relationships with industry. Co-authors disclosed relationships with F. Hoffmann-La Roche, Biogen, Geras Solutions, AVID Radiopharmaceuticals, Eli Lilly, Eisai, GE Healthcare, Pfizer, Genentech, Siemens, Alzpath, and Cerveau.

Peters and Nacmias disclosed no relationships with industry.

Primary Source

Neurology

Source Reference: Glans I, et al "Association between dietary habits in midlife with dementia incidence over a 20-year period" Neurology 2022; DOI: 10.1212/WNL.0000000000201336.

Secondary Source

Neurology

Source Reference: Peters N and Nacmias B "Does diet matter? The implications of dietary habits for dementia" Neurology 2022; DOI: 10.1212/WNL.0000000000201420.

How diet affects Alzheimer's disease and small vessel disease

 But you give us nothing specific, so useless.

How diet affects Alzheimer's disease and small vessel disease

Juha Lempiäinen

First published: 28 March 2022

https://doi.org/10.1002/lim2.57

Abstract

Introduction

The number of people with memory disorders is increasing worldwide. Changing certain lifestyle factors can prevent the development of those disorders. Diet is a central factor that can be changed.

Methods

A systematic literature search was conducted to identify peer-reviewed articles that examined the relationship between a plant-based diet and Alzheimer's disease or SVD.

Results

Whole-food, plant-based diets also seem to be a healthy choice for the brain. Berries, vegetables and fibre seem to be especially important. The amounts of saturated fat, refined carbohydrates and alcohol should be minimised. Single components (dietary supplements) are not beneficial if one has no deficiencies.

Conclusions

A plant-based diet containing plenty of fibre, vitamins, and polyphenols seems to be a good choice for our memory and brain health.

1 INTRODUCTION

The number of memory disorders grows as people age. This causes many lost work years and lowers their quality of life now and in the future. Alzheimer's disease, in which beta-amyloid accumulates in the neurons, is a common cause of dementia. About 50 million people suffer from this disease globally, and the number is estimated to more than double by 2050.¹ Cerebral small vessel disease (SVD) is a major cause of vascular memory disorders.² Alzheimer's and SVD are present simultaneously in many cases and cause the so-called mixed dementia. Memory disorders decrease the quality of life, whatever their underlying cause is. People also lose many healthy working years, making these diseases very expensive for society. Many countries already have national guidelines for the prevention and treatment of these diseases.³ However, more information about lifestyle factors that affect the prevention and treatment of these diseases should also be included in these guidelines.

The published results of the Finnish FINGER study quite recently showed that losing one's memory can be effectively prevented with lifestyle changes.⁴ Study participants in this multidomain intervention received information on a healthy diet, and the intervention group also received nutritional guidance both individually and in groups. The intervention group also met with a nurse and a physician for management of vascular risk factors, increased exercise and cognitive training. Thus, we cannot know for sure the individual effects of any dietary changes. However, epidemiological studies have shown that diet is related to a risk of memory disorders. It is important to observe that it is hard to show direct causality in epidemiological studies between food choices and memory because often those people who eat healthily are also non-smokers who have other potentially protective habits such as exercising.⁵

However, according to the FINGER study researchers, ‘Elderly people should eat more vegetables, fruits, berries, fish and whole grains and increase also amounts of vegetable fats and vitamin D… It [is] also important to encourage [them] to quit smoking and not to drink alcohol’.⁶ We cannot say for sure, but the results of this intervention study indicate that a plant-based diet that contains fibre and vegetable fats seems to be good for brain health and memory. A follow-up study from this same cohort (and other intervention and follow-up studies) will probably show more detailed information about how single nutritional factors influence cognition/memory and the risk they pose for memory diseases. This article reviews the current knowledge of these single components of our diet and their effects on the development and treatment of Alzheimer's disease and cerebral SVD.

A systematic literature search was conducted using PubMed to identify peer-reviewed articles that examined the relationship between a plant-based diet and Alzheimer's disease or SVD in the past 14 years (2006–2020). The exact search date range was 1 January 2006, through 31 December 2020. Google searches were performed to identify additional articles that may have been missed in the database search. A Boolean search strategy was conducted with the following keywords and logic: (‘diet’ or ‘dietary patterns’ or ‘dietary factors’ or food’ or ‘nutrition’ or ‘plant based’ or ‘whole food plant based’ or ‘WFPB’ or ‘Mediterranean diet’) and (‘Alzheimer's disease’ or ‘dementia’ or ‘SVD’ or ‘cerebral SVD’ or ‘cognitive impairment’ or ‘cognitive decline’).

A study was included in the review if, according to its abstract, it provided information about a relationship between a plant-based diet and memory disorders (Alzheimer's disease, SVD or cognitive impairment). No limitations were set on a study's setting or country. Studies whose authors had potential conflicts of interest were excluded. Five studies were selected after screening all abstracts based on these criteria, and the references of the studies were additionally screened to identify eligible studies. On the basis of the aforementioned exclusion and inclusion criteria, a total of 33 studies were identified and included in this systematic review. Two more articles were included in the revision phase according to the reviewers’ comments.

 

More at link.

 

Brain Aging Markers Tied to Inflammatory Foods

 Way too generic to be useful at all. I expect your doctor and hospital to have EXACT DIET PROTOCOLS.

We need protocols for all these:

For stroke prevention; for dementia prevention; for cognitive improvement; for cholesterol reduction; for plaque removal; for Parkinsons prevention; for inflammation reduction; for blood pressure reduction. 

THIS IS YOUR DOCTOR'S RESPONSIBILITY! Why are you giving them a pass? Guidelines don't count.

Brain Aging Markers Tied to Inflammatory Foods

Smaller brain volume seen with diet-driven inflammation

by Judy George, Senior Staff Writer, MedPage Today May 13, 2022

Diets high in inflammatory foods were linked with global markers of brain aging and cerebral small vessel disease on MRI, a cross-sectional study showed.

Compared with anti-inflammatory diets, those considered pro-inflammatory on the Dietary Inflammatory Index (DII) were associated with smaller total brain volume (beta -0.16, P<0.0001) after adjusting for demographic, clinical, and lifestyle covariates, according to epidemiologist Debora Melo van Lent, PhD, a postdoctoral researcher at UT Health San Antonio in Texas, and co-authors.

Higher DII scores -- indicating more pro-inflammatory foods -- were also associated with smaller total gray matter volume (beta -0.08, P=0.003) and larger lateral ventricular volume (beta 0.04, P=0.03), the researchers reported in Alzheimer's & Dementia. No associations were seen with other brain MRI measures.

"Systemic inflammatory processes in the body, including the brain, can be influenced by diet, leading to its important contributory role in brain aging," the researchers observed.

"In our study we found evidence of an association between DII scores and global markers of brain volumes and vascular brain injury, which are early markers of dementia," they wrote. "Moreover, previous studies have shown associations between the DII and risk factors of dementia. Our findings indicate potential for prevention by dietary modification."

The DII index used in the study consisted of 31 dietary components including anti-inflammatory nutrients, pro-inflammatory nutrients, whole foods, and caffeine from food intake. Dietary components were categorized as:

• Anti-inflammatory: alcohol, beta carotene, caffeine, dietary fiber, folic acid, magnesium, thiamine, riboflavin, niacin, zinc, monounsaturated fat, polyunsaturated fat, omega-3 fat, omega-6 fat, selenium, vitamins B6, A, C, D, E, green/black tea, pepper, and garlic
• Pro-inflammatory: vitamin B12, iron, carbohydrates, cholesterol, total energy intake, protein, saturated fat, and total fat

In previous research, diets with high inflammatory potential had been tied to dementia or cognitive impairment, but there's limited research about diet-driven inflammation and early MRI markers of neurodegeneration and vascular brain damage, Melo van Lent and co-authors said.

"The relationship between the energy-adjusted DII and structural MRI outcomes of brain aging has been investigated only once in a small study sample; no significant relationships were found," they wrote.

Melo van Lent and colleagues studied 1,897 participants in the Framingham Heart Study Offspring cohort who completed food frequency questionnaires and underwent brain MRI scans. Food frequency questionnaire data were collected several times over a decade and DII scores were averaged over a mean period of 7 years.

Participants had an average baseline age of 62 years; about 54% were women and 23% carried an apolipoprotein E ε4 (APOE4) allele. People with prevalent dementia, stroke, or significant neurological disease were excluded.

The mean DII score was -0.26, indicating that diets in the group on average were anti-inflammatory relative to the global mean in the DII world database. Overall, higher DII scores were not associated with regional markers of brain aging, but some results differed by APOE4 status and sex. DII scores were associated with smaller hippocampal volume in people with no APOE 4 allele and with larger white-matter hyperintensity volume in men.

The most pro-inflammatory components of the Dietary Inflammatory Index -- saturated fat, trans fats, and total energy intake -- also contribute to worse vascular health when consumed in abundance, the researchers noted.

"Fortunately, replacement of saturated fats with other macronutrients, such as polyunsaturated fats (i.e., anti-inflammatory), has been related to a reduced risk for cardiovascular disease, offering a promising opportunity for reducing risk for dementia," they wrote.

The analyses had several limitations, Melo van Lent and co-authors acknowledged. It relied on food frequency questionnaires, which are subject to measurement error and recall bias. In addition, the study population consisted of white individuals of European ancestry and results may not apply to other groups.

"Replication studies are needed across diverse populations," they wrote. "In addition, research should investigate the impact of the DII across different subgroups at risk for dementia, including persons who are carriers/non-carriers of the apolipoprotein E ε4 gene, and men and women."

• Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

This study was supported by the National Heart, Lung, and Blood Institute, the National Institute on Aging, the National Institute of Neurological Disorders, the Agricultural Research Service Agreement, and the ASPEN Rhoads Research Foundation.

Melo van Lent is vice-chair of the Alzheimer's Association ISTAART Nutrition Metabolism and Dementia Professional Interest Area.

One co-author is part of the Danone North America Essential Dairy and Plant-Based Advisory Board.

Primary Source

Alzheimer's & Dementia

Source Reference: Melo van Lent D, et al "Higher Dietary Inflammatory Index scores are associated with brain MRI markers of brain aging: Results from the Framingham Heart Study Offspring cohort" Alzheimer's Dement 2022; DOI: 10.1002/alz.12685.

 

Can Certain Foods Really Stave Off Dementia?

 At the NYTimes. I didn't learn anything new here, but this pithy saying: 

Instead, Dr. Petersen, of the Mayo Clinic, said, remember this pithy adage: “If it comes from a plant, eat it. If it’s made in a plant, don’t eat it.

Can Certain Foods Really Stave Off Dementia?

Two servings of avocado per week may lower risk for CVD, CHD but not stroke

 Up to you to figure out what to do with this, your doctor is not present for any protocol to do with diet.

Two servings of avocado per week may lower risk for CVD, CHD but not stroke

By Scott Buzby

You'll

Two servings of avocado per week, compared with not eating any avocado, was associated with lower risk for CVD and CHD, but not stroke, researchers reported.

According to data published in the Journal of the American Heart Association, replacing half of one daily serving of margarine, butter, egg, yogurt, cheese or processed meats with avocado was tied to lower risk for CVD.

Data were derived from Pacheco LS, et al. J Am Heart Assoc. 2022;doi:10.1161/JAHA.121.024014.

“Avocados are a nutrient-rich food item with favorable bioactive food compounds including monounsaturated and polyunsaturated healthy fats, soluble fiber, vegetable proteins, phytosterols and polyphenols and there are potential biological mechanisms by which avocados offer cardioprotective benefits, which is through modulating CV risk factors,” Lorena S. Pacheco, PhD, MPH, RDN, postdoctoral research fellow in the nutrition department at the Harvard T.H. Chan School of Public Health, told Healio. “The primary monounsaturated fatty acid present in avocados is oleic acid, and it is suggested that it helps in reducing hypertension, inflammation and insulin sensitivity. Additionally, they contain plant sterols, that could have favorable effects on lipid profiles. Moreover, the soluble fiber intake in avocados can also lead to a better lipid profile.”

The researchers reported that the Hass avocado, the most consumed variety in the U.S., contains approximately 13 g of oleic acid in a medium-sized fruit, which is comparable to the amount of oleic acid in 1.5 oz of almonds or 2 tablespoons of olive oil. Additionally, half of an avocado contains approximately 20% of the daily recommended fiber, 10% of daily recommended potassium, 5% of daily recommended magnesium and 15% of daily recommended folate.

“This study aimed to examine the association between avocado consumption with CVD, which includes CHD and stroke,(You're that fucking out-of-date that you missed that

(stroke has been called neurological disease by the WHO since 2006)

instead of CVD? And you're still employed in the medical field?) in two large U.S. prospective cohort studies,” Pacheco told Healio. “We also wanted to estimate the risk of CVD, CHD and stroke when we substitute different fat-containing food sources with the same amount of avocado.”

CV effects of weekly avocado intake

Researchers included 68,786 women from NHS and 41,701 men from HPFS who had no cancer, CHD or stroke at baseline. Avocado intake was evaluated using validated food frequency questionnaires at baseline and then every 4 years. Median follow-up was approximately 13 years for women and 14 years for men.

Overall, participants with higher avocado consumption also had higher total energy intake and diet quality, including greater intake of fruits, vegetables, whole grains, nuts and dairy products compared with those with lower avocado consumption.

For the present analysis, half of an avocado was classified as a single serving.

Researchers reported that individuals who ate at least two servings of avocado per week experienced 16% lower risk for CVD (HR = 0.84; 95% CI, 0.75-0.95; P for trend = .0007) and 21% lower risk for CHD (HR = 0.79; 95% CI, 0.68-0.91; P for trend < .001) compared with those who did not consume avocado. However, they observed no association between avocado intake and risk for stroke (P for trend = .78).

“We defined CVD as the composite of fatal CHD and nonfatal MI and fatal and nonfatal stroke,” Pacheco told Healio. “Thus, we did find an association with CVD but not with stroke, meaning that the risk of CVD is primarily driven by CHD. As my co-authors and I discuss in the paper, our stroke findings could be explained by chance or the lack of statistical power in our models.”

For every half-serving increase in avocado intake per day, researchers observed an approximately 20% lower risk for CVD (HR = 0.8; 95% CI, 0.71-0.91), according to the study.

Moreover, replacing half of one daily serving of margarine, butter, egg, yogurt, cheese or processed meats with a half serving of avocado was associated with a 16% to 22% lower risk for CVD, according to the study.

“We know avocados impart heart-healthy benefits. Yet, avocados are also calorie-rich, so pairing them with chips or the like compromises those benefits since we need to consider your portion of avocado and your portion of chips,” Pacheco told Healio. “In most cases, when you have guacamole or similar spreads, it is easy to overconsume them, increasing your overall calories. Besides this, most of us do not pay attention to the serving size on the bag of chips and keep ‘munching away’, making this a troublesome combination.”

Benefits of a routine healthy diet

“We desperately need strategies to improve intake of AHA-recommended healthy diets — such as the Mediterranean diet — that are rich in vegetables and fruits,” Cheryl Anderson, PhD, MPH, FAHA, professor and dean of the Herbert Wertheim School of Public Health and Human Longevity Science at University of California, San Diego, and chair of the AHA Council on Epidemiology and Prevention, said in the release. “Although no one food is the solution to routinely eating a healthy diet, this study is evidence that avocados have possible health benefits. This is promising because it is a food item that is popular, accessible, desirable and easy to include in meals eaten by many Americans at home and in restaurants.”

Read next

Reducing sodium, increasing potassium intake may cut CV risk
Simple food swaps may lower stroke risk

Reference:

• Eating two servings of avocados a week linked to lower risk of cardiovascular disease. newsroom.heart.org/news/eating-two-servings-of-avocados-a-week-linked-to-lower-risk-of-cardiovascular-disease. Published March 30, 2022. Accessed March 30, 2022.