Standing on one leg is the most reliable indicator of aging.

The longer you can maintain your balance, the better.

A recent study has shown these results. Doctors compared several parameters of neuromuscular aging and found out which of them correlates most strongly with age. The observation was carried out on women and men over 50 years old - without obesity, neuromuscular disorders, spinal pathologies and other ailments that affect everyday activities.

Over 10 years...

🔜 The ability of the study participants to stand in the heron pose (on one leg) decreased by an average of 2.2 seconds for the non-dominant leg and by 1.7 for the dominant one.
🔜 The grip strength in the dominant hand decreased by 3.7%
🔜 The knee extension strength decreased by 1.4%.

✖️Scientists called gait the most unsuccessful indicator of neuromuscular aging, since its changes were weakly dependent on age.

Gender differences were present only in strength indicators, but did not affect balance. With age, the center of pressure shifted significantly in both men and women. Moreover, the ability to remain in the heron pose deteriorated the most in comparison with other indicators.

Standing on one leg - sounds easy. But you try 🙂 Stand on one leg, close your eyes.

If you stood...

30 seconds - you are about 20 years old;
15 seconds - less than 40;
4-5 seconds - 60 years and older.
(the test is based on the Romberg neurological test)

How long could you hold on?

In the picture:
Duration of standing on one leg for (a) non-dominant (R2 = 0.38, p < 0.001) and (b) dominant (R2 = 0.27, p = 0.004) sides.

The results were remarkable. First, subjects with Lewy body disease had no cognitive benefit from treatment. However, those with Alzheimer’s disease who received an AChEI had almost no change in the MMSE score for six years while subjects not taking an AChEI continued to decline. At the end of follow up in year twelve, subjects with Alzheimer’s taking an AChEI had a 5.7 decrease in MMSE score from onset compared to those not taking an AChEI who decreased an average of 10.8 points. Keep in mind that the top score on the MMSE is 30 and the cutoff for dementia is 23 and below, so the AChEI treated subjects, shown on the red line, had on average remained above the dementia cutoff until near the end of the study.

The same pattern although not as pronounced was seen in subjects with vascular dementia. I suspect this reflects the high incidence of comorbidity: nearly a half of dementia brains seen at autopsy have both Alzheimer’s and vascular dementia pathology.

In addition to the slowing of cognitive decline, there was a strong association between AChEI therapy and lower all-cause mortality. This was true even for subjects with Lewy body disease who had no cognitive benefit from taking AChEI drugs. This suggests to me that the increased survival associated with these drugs must have a different mechanism than that resisting cognitive decline. https://www.reddit.com/r/AlphaCognition/comments/1auhnv3/surprisingly_good_news_about_the/

As of November 2024, several human clinical trials are actively investigating interventions aimed at promoting longevity and healthy aging. Notable ongoing studies include:

1. Metformin Trials: The Targeting Aging with Metformin (TAME) trial is a series of nationwide, six-year clinical trials at 14 leading research institutions across the country that will engage over 3,000 individuals between the ages of 65-79. These trials will test whether those taking metformin experience delayed development or progression of age-related chronic diseases—such as heart disease, cancer, and dementia. ([Afar](https://www.afar.org/tame-trial))

2. Rapamycin Studies: The Participatory Evaluation of Aging with Rapamycin for Longevity (PEARL) study is a large-scale, placebo-controlled clinical trial designed to assess the effects of rapamycin on human aging and longevity. The study evaluates the safety and efficacy of rapamycin in mitigating clinical signs of aging in a normative aging cohort. ([MedRxiv](https://www.medrxiv.org/content/10.1101/2024.08.21.24312372v1))

3. Caloric Restriction Studies: The Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE) trial investigates the effects of prolonged calorie restriction on healthy human subjects, aiming to assess its impact on lifespan and healthspan. The study assesses the effects of caloric restriction on metabolic and physiological functions. ([Frontiers](https://www.frontiersin.org/journals/aging/articles/10.3389/fragi.2022.820215/full))

4. Human Longevity Laboratory Initiatives: The Human Longevity Laboratory at Northwestern Medicine conducts multidimensional phenotyping to measure biological age in participants, with plans to launch clinical trials testing interventions that may slow or reverse aging processes. The laboratory aims to develop and test interventions that target the aging process. ([Frontiers](https://www.frontiersin.org/journals/aging/articles/10.3389/fragi.2022.820215/full))

These studies represent a concerted effort to understand and potentially modulate the aging process in humans through various pharmacological and lifestyle interventions.

Imagine with all humanity/s achievements in different industries, we, humans, made less than 5 human trials for life etention, And if today we will launch a new longevity drug or intervention in will take up to 15 years to verify its potential with 7,9% chance that it will succeed.

While all people are busy with earning money the "asteroid is coming to kill us all", with small chance to stop it

https://pmc.ncbi.nlm.nih.gov/articles/PMC10173933/#:~:text=Clinical%20trials%20are%20an%20essential,high%20risk%20for%20biopharmaceutical%20companies.

If you want to change it,join Longevity InTime company

If you still don’t get it, watch this:

https://youtu.be/vN2yLmlUQsk?si=Ifmavpy9D41kWFO-

https://www.cancerresearchuk.org/about-cancer/find-a-clinical-trial/how-clinical-trials-are-planned-and-organised/how-long-it-takes-for-a-new-drug-to-go-through-clinical-trials#:~:text=There%20is%20no%20typical%20length,a%20drug%20to%20be%20licensed.

Maximum number of recommendations for reducing Alzheimer’s:

Dementia is the main reason behind the Alzheimer’s disease. One has to follow MIND diet or Mediterranean diet that has low blood pressure, provides cognitive benefits.
The changes inside the brain will begin at the early stages only. This can be prevented by diet, taking different lifestyle and supplements. Diseases that are related to Alzheimer’s like obesity, diabetes helps in the increasing of Alzheimer’s risk.
Usually, food which contains less red meat, eggs and sweets have less risk of this disease. When compared the MIND (Mediterranean intervention for neurodegenerative delay) with the western form of food diet, MIND has shown good results. It includes leafy vegetables, nuts, fish, grains, olive oil…etc. Over 900 adult individuals have gone to be dementia free.
Scientists are finding the perfect reason why MIND diet is best for the reduction of dementia. It is found that it helps in reducing cardiovascular risk which is high in western diet. It is also proven that the eye-related diseases are also reduced.
Foods like blueberries, leafy vegetables have potential cognitive benefit. Because they have slower age effect. Same is found on the fish.

Vitamins and supplements:
Many observational studies have said that vitamin B, E are helpful in Alzheimer’s and cognitive health. DHA supplement like omega-3 fatty acid found in fatty fish is proven to be helpful. But in human trials it is not proven successful. In a study for 4,000 adults, it is found that there is no help in cognitive decline.
At present time, no drug is proven to be successful in curing Alzheimer’s disease. Although there are so many medicines in internet and drug stores, there is no valid proof that it works. Deficiency of B12 is the biggest reason for memory problems.
Ketogenic diet is also said to be helpful for brain to keep energy to brain cells, to use energy for overall function. Researchers are still finding a perfect diet for prevention of dementia.
Link - https://www.nia.nih.gov/health/what-do-we-know-about-diet-and-prevention-alzheimers-disease

Treating the symptoms of Alzheimer’s can help provide people with comfort, dignity, and independence for a longer period of time and assist their caregivers. Galantamine, rivastigmine, and donepezil are cholinesterase inhibitors that are prescribed for mild to moderate Alzheimer’s symptoms. These drugs may help reduce or control some cognitive and behavioural symptoms.

FDA-approved medications to treat Alzheimer's:
•Lecanemab:
Disease-modifying immunotherapy. Treats mild cognitive impairment or mild Alzheimer’s by removing abnormal beta-amyloid to help reduce the number of plaques in the brain. Possible side effects include brain swelling and bleeding, headache, cough, diarrhea, nausea, vomiting, fever, chills, body aches, fatigue, high blood pressure, low blood pressure, and low oxygen. Delivered through IV over one hour every two weeks.
FDA Accelerated Approval to treat Alzheimer's:
•Aducanumab:
Disease-modifying immunotherapy. Treats mild cognitive impairment or mild Alzheimer’s by removing abnormal beta-amyloid to help reduce the number of plaques in the brain. Possible side effects include brain swelling and bleeding, headache, dizziness, falls, diarrhea, and confusion. Delivered through IV over one hour every four weeks.
FDA-approved medications to manage symptoms:
Galantamine:
Cholinesterase inhibitor. Treats symptoms of mild to moderate Alzheimer’s by preventing the breakdown of acetylcholine and stimulates nicotinic receptors to release more acetylcholine in the brain. Possible side effects include nausea, vomiting, diarrhea, decreased appetite, weight loss, dizziness, and headache. Delivered through an extended-release capsule taken once a day or through a tablet or liquid taken twice a day.
Rivastigmine:
Cholinesterase inhibitor. Treats symptoms of mild, moderate, and severe Alzheimer’s by preventing the breakdown of acetylcholine and butyrylcholine (a chemical similar to acetylcholine) in the brain. Possible side effects include nausea, vomiting, diarrhea, weight loss, indigestion, decreased appetite, anorexia, and muscle weakness. Delivered through a capsule twice a day or through a skin patch that is replaced once a day.
Link - https://www.nia.nih.gov/health/how-alzheimers-disease-treated#:~:text=Medications%20for%20mild%20to%20moderate%20Alzheimer's%20disease,-Treating%20the%20symptoms&text=Galantamine%2C%20rivastigmine%2C%20and%20donepezil%20are,some%20cognitive%20and%20behavioral%20symptoms.

Staying mentally and socially active:
There's some evidence to suggest that rates of dementia are lower in people who remain mentally and socially active throughout their lives.
It may be possible to reduce your risk of Alzheimer's disease and other types of dementia by:
Reading
Learning foreign languages
Playing musical instruments
Volunteering in your local community
Taking part in group sports, such as bowling
Trying new activities or hobbies
Maintaining an active social life
Link - https://www.nhs.uk/conditions/alzheimers-disease/prevention/

Risk factors that cannot be changed
Age, biological sex and genetics are Alzheimer’s risk factors beyond our control. Adults over 65 and women are at higher risk for developing Alzheimer’s disease. For these high-risk individuals, the 10 early signs and symptoms of Alzheimer’s provide a good foundation for a conversation to have with your healthcare provider, said Lenette Jones, Ph.D., R.N., the Nancy S. and Michael B. McLelland Professor of Nursing and assistant professor at the University of Michigan School of Nursing.
“If you have any questions or memory concerns, that’s a good starting point,” Jones said.
Certain genetic predispositions place individuals at higher risk of developing Alzheimer’s disease.
“We all have the APOE gene, but one in four of us have a variant called APOE4 that increases the chances of developing Alzheimer’s,” Roberts said.
“If someone has one or two copies of the APOE4 inherited from their parents, then they are at elevated risk for Alzheimer’s. Genetic factors are relevant, but they aren’t destiny. You can have the APOE4 allele and still never get the disease, and you can get the disease without having that specific genetic variant.”
Link - https://www.michiganmedicine.org/health-lab/what-you-can-do-now-prevent-alzheimers-disease

Foods to Eat on the MIND Diet

Green leafy vegetables (kale, spinach, collard greens, lettuce): a minimum of 6 servings a week
Nuts (almonds, cashews, pistachios): a minimum of 5 servings a week
Berries (strawberries, blueberries, raspberries, blackberries): a minimum of 2 servings a week
Beans (black beans, pinto beans, kidney beans): a minimum of 3 servings a week
Whole grains (quinoa, oatmeal, brown rice, whole-grain pasta and bread): a minimum of 3 servings a day (5)
Fish (salmon, tuna, trout): at least 1 serving a week.
Poultry (chicken, turkey): at least twice a week
Olive oil as the primary oil used.
Wine: no more than 1 glass a day
Foods to Limit on the MIND Diet
Red meat (steak, ground beef, pork, lamb): no more than 4 servings a week
Butter and margarine: no more than 1 tablespoon daily
Cheese (brie, mozzarella, or cheddar): no more than 1 serving a week.
Sweets (cakes, brownies, ice cream): no more than 5 servings a week
Fried or fast food (french fries, chicken nuggets, onion rings, fried chicken, hamburgers): no more than 1 serving a week.

Sleeping pill reduces levels of Alzheimer’s proteins:

Sleep disturbances can be an early sign of Alzheimer’s disease. Many people eventually diagnosed with Alzheimer’s start having trouble falling and staying asleep years before cognitive problems such as memory loss and confusion emerge. It’s a vicious cycle: Alzheimer’s disease involves changes to the brain that disrupt sleep, and poor sleep accelerates harmful changes to the brain.
Researchers at Washington University School of Medicine in St. Louis have identified a possible way to help break that cycle. A small, two-night study has shown that people who took a sleeping pill before bed experienced a drop in the levels of key Alzheimer’s proteins — a good sign, since higher levels of such proteins tracks with worsening disease. The study, which involved a sleeping aid known as suvorexant that is already approved by the Food and Drug Administration (FDA) for insomnia, hints at the potential of sleep medications to slow or stop the progression of Alzheimer’s disease, although much more work is needed to confirm the viability of such an approach.

As a first step to assess the effect of orexin inhibitors on people, Lucey and colleagues recruited 38 participants ages 45 to 65 and with no cognitive impairments to undergo a two-night sleep study. The participants were given a lower dose (10 mg) of suvorexant (13 people), a higher dose (20 mg) of suvorexant (12 people) or a placebo (13 people) at 9 p.m. and then went to sleep in a clinical research unit at Washington University. Researchers withdrew a small amount of cerebrospinal fluid via spinal tap every two hours for 36 hours, starting one hour before the sleeping aid or placebo was administered, to measure how amyloid and tau levels changed over the next day and a half.

In the cerebrospinal fluid of people who had received the high dose of suvorexant, amyloid levels dropped 10% to 20% and levels of a key form of tau known as hyperphosphorylated tau dropped 10% to 15%, compared to people who had received placebo. Both differences are statistically significant. There was not a significant difference between the people who received a low dose of suvorexant and those who received the placebo.

The study is preliminary, since it only looked at the effect of two doses of the drug in a small group of participants. Lucey has studies underway to assess the longer-term effects of orexin inhibitors in people at higher risk of dementia.
“Future studies need to have people taking these drugs for months, at least, and measuring the effect on amyloid and tau over time,” Lucey said. “We’re also going to be studying participants who are older and may still be cognitively healthy, but who already have some amyloid plaques in their brains. This study involved healthy middle-aged participants; the results may be different in an older population.

LINK - https://medicine.wustl.edu/news/sleeping-pill-reduces-levels-of-alzheimers-proteins/

Drinking coffee may reduce the risk of developing Alzheimer’s disease:
The study involved 227 adults aged 60 years or over, who did not have cognitive decline at the start of the study. The team used a questionnaire to gather information from the participants about the amount and frequency of coffee they consumed.
They then performed cognitive assessments using a selection of psychological measures at baseline and 18-month intervals. These assessments measured six cognitive areas: episodic recall memory, recognition memory, executive function, language, attention and processing speed, and the AIBL Preclinical Alzheimer Cognitive Composite (PACC).

Analysis of the data showed that habitual coffee drinking was positively associated with the cognitive areas of executive function, attention, and the PACC score. Drinking higher amounts of coffee was associated with slower cognitive decline in these areas over the course of the study.
Higher baseline coffee consumption was also linked to a slower accumulation of amyloid protein over the 126 months.
There did not seem to be a link between coffee intake and brain volume atrophy in this study.
The observed results suggest that increasing coffee intake from 1 to 2 cups per day could potentially reduce cognitive decline by up to 8% after 18 months. There could also be up to a 5% decrease in cerebral beta-amyloid accumulation over the same period.
Dr. Gardener told MNT, “[h]igher coffee intake was associated with slower accumulation of the sticky protein called beta-amyloid, which clumps together in the brains of those with Alzheimer’s disease.”
LINK - https://www.medicalnewstoday.com/articles/drinking-coffee-may-reduce-the-risk-of-developing-alzheimers-disease#Investigating-the-link

Homotaurine – failed as Alzheimer’s drug, now used for memory protection:
Only 20% of the drugs that begin Phase I clinical trials ever get to market.1 The other 80%, despite the millions of dollars spent in research and development, are part of the cost of doing business for the pharmaceutical industry. One Canadian-based company is now taking the extraordinary step of trying to recoup this cost by marketing as a neutraceutical a drug that the Food and Drug Administration (FDA) refused to approve for marketing in the United States.2
OVOS Natural Health Inc., a subsidiary of Bellus Health Inc. (formerly known as Neurochem), has brought homotaurine, a modification of the amino acid taurine, to market under the trade name Vivimind. In clinical trials, this agent—studied for the treatment of Alzheimer’s disease (AD)—is also known as 3-amino-1-propane-sulfonic acid (3-APS), tramiprosate, and Alzhemed. Vivimind is currently being marketed in Canada and on the Internet to healthy baby boomers for memory protection. According to a representative from OVOS, Vivimind was to be accessible to U.S. residents in 2009 (OVOS Natural Health, personal communication, 2009 Jan 13). The following is a brief discussion on the history of this agent and a commentary on the decision to market it as a nutraceutical.
Link - https://academic.oup.com/ajhp/article-abstract/66/21/1950/5130452?redirectedFrom=fulltext
Apolipoprotein E (ApoE) genotype is the major genetic risk factor for late-onset AD. The APOE ε4 allele confers a 4- to 12-fold higher risk of AD and lowers the age of onset by ~10–15 years (15, 16). The ApoE ε4 allele may also play a role in early-onset AD, delaying the onset of symptoms (17), and in other neurodegenerative diseases, where APOE ε4 status is a risk factor for co-pathology and poor evolution (18). ApoE protein binds to soluble Aβ and affects aggregation, transport, and clearance of amyloid within the central nervous system (CNS), increasing Aβ oligomers in the brain, which would contribute to the loss of dendritic spines thus accelerating memory impairment and leading to earlier cognitive decline in AD (16, 19, 20).
Homotaurine (tramiprosate) :
Evidence Summary:
Although tramiprosate failed in a phase 3 clinical trial, a post-hoc analysis showed benefits in ApoE4 individuals.
Neuroprotective Benefit:
Phase 3 studies in Alzheimer’s patients failed to show a benefit with tramiprosate, but a sub-group analysis in ApoE4 individuals shows some promise.
Aging and related health concerns: N/A
Safety: Tramiprosate is associated with a number of mild side effects, mostly gastrointestinal in nature.
What is it?
Homotaurine (tramiprosate) was discovered in a screen for small molecules that inhibit amyloid beta aggregation. It is structurally similar to taurine except that it has an extra carbon. It was the first phase 3 study to test the ‘amyloid hypotheses. Although tramiprosate failed in phase 3 clinical trials, a subgroup analysis showed that it stabilized cognition in ApoE4 individuals.
Neuroprotective Benefit:
Phase 3 studies in Alzheimer’s patients failed to show a benefit with tramiprosate, but a sub-group analysis in ApoE4 individuals shows some promise.
Types of evidence:
• One phase 2 and two phase 3 studies in Alzheimer’s patients.
• One preclinical study.

A phase 2 study of 58 patients reported a dose dependent decrease in CSF Aβ42 over three months (up to 70% reduction from baseline in 150mg group) (Aisen et al, 2006). This is odd considering tramiprosate’s proposed mechanism of action is to prevent amyloid aggregation (a drug that reduced the aggregation of amyloid beta would expectedly increase CSF levels as amyloid is cleared) (Karran and Hardy, 2014). However, there were no differences in CSF Aβ40 or total tau. In an 18-month phase 3 study of 790 patients with mild-to-moderate Alzheimer’s disease, tramiprosate (100mg or 150mg bid) failed to provide cognitive benefits (Aisen et a, 2011). There was, however, a trend for less hippocampal volume loss. The study was powered to detect a 25% reduction in cognitive loss. For an unknown reason, there was a lot of variability between the study sites and the placebo group deteriorated less than is historically common. Therefore, the authors concluded that the study was insufficiently powered. Regardless, because of the failure in the trial, the company stopped another ongoing phase 3 study in Europe.
ApoE4:
Subgroup analyses of the two phase 3 trials reported a gene-dose effect with tramiprosate, showing no cognitive effect in ApoE4 non-carriers, intermediate benefits in ApoE4 heterozygotes, and the greatest cognitive benefit in ApoE4 homozygotes. In addition, patients on the higher dose of tramiprosate (150mg bid) and with mild (vs. moderate) Alzheimer have responded better to the drug. In fact, cognition in mild Alzheimer’s ApoE4 homozygotes stabilized with tramiprosate and was 40% better than placebo, which the authors claim is clinically meaningful. The authors speculate that since tramiprosate’s mechanism of action is to prevent amyloid aggregation, and since ApoE4 patients have a higher amyloid burden, it would be most beneficial in this group.
Safety:
Tramiprosate is associated with a number of mild side effects, mostly gastrointestinal in nature.
Types of evidence:
• One phase 2 and two phase 3 studies in Alzheimer’s patients
The most common side effects of tramiprosate are gastrointestinal in nature (nausea and vomiting) and can occur in up to 23% of the patients on the drug (compared to 13% in placebo). However, they tend to be mild and moderate in nature. Syncope, pneumonia, and weight loss were also more common in the drug group (occurring in 3.8%, 2.3%, and 15% of patients, respectively) (Aisen et al, 2011). ApoE4 homozygotes also had an increased incidence of depression (13% vs. 9% for placebo) (Abusharkra et al, 2017). It is unclear what caused these drug effects in patients. Tramiprosate was not associated with Amyloid Related Imaging Abnormalities (ARIA) – abnormalities present on the MRI scans of some patients with other amyloid-related drugs.
Drug Interactions:
There is no information on potential drug interactions.
Availability/Dosing:
After the failure of phase 3 clinical trials, tramiprosate began to be sold as a supplement called VIVImind (later ActiveMind from Advances Orthomolecular Research). In clinical studies best results were seen at doses of 150mg twice per day.
Research underway:
Alzheon purchased the rights to tramiprosate after the failed clinical trials and created a new pro-drug ALZ-801 that is reported to have improved pharmacokinetics, tolerability, and metabolic stability. Although not listed on clinicaltrials.gov, Alzheon’s website reports that it is currently in phase 2 clinical trials for ApoE4 homozygotes and heterozygotes.
Link - https://www.alzdiscovery.org/uploads/cognitive_vitality_media/Homotaurine-tramiprosate-Cognitive-Vitality-For-Researchers.pdf

Approximately 25% of the general population carries at least one ε4 allele of the Apolipoprotein E (APOE ε4), the strongest genetic risk factor for late onset Alzheimer’s disease. Beyond its association with late-onset dementia, the association between APOE ε4 and change in cognition over the adult life course remains uncertain. This study aims to examine whether the association between Apolipoprotein E (APOE) ε4 zygosity and cognition function is modified between midlife and old age.
Compared to non-carriers, heterozygote (prevalence 25%) and homozygote (prevalence 2%) APOE ε4 carriers had increased risk of dementia, sub-distribution hazard ratios 2.19 (95% CI 1.73, 2.77) and 5.97 (95% CI 3.85, 9.28) respectively. Using data spanning 45–85 years with non-ε4 carriers as the reference, ε4 homozygotes had poorer global cognitive score starting from 65 years; ε4 heterozygotes had better scores between 45 and 55 years, then no difference until poorer cognitive scores from 75 years onwards. In analysis of individual cognitive tests, better cognitive performance in the younger ε4 heterozygotes was primarily attributable to executive function.
The ε4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late onset Alzheimer’s disease (AD) [1]. Around 25% of the Caucasian population carries at least one ε4 allele [2], with a 3-fold increased risk of AD for heterozygotes and a nearly 15-fold increased risk for homozygotes compared to the ε3 homozygotes, the most common genotype [3].
The mechanisms underlying the relationship between APOE ε4 and AD are thought to be complex [5], involving, e.g., β-amyloid (Aβ) peptide clearance [6], neuronal death [7], and phosphorylation of tau [8].
In addition to AD, APOE ε4 plays a role in other causes of dementia, including vascular dementia [9], and Lewy Body disease [10]. Although case-control and longitudinal studies have examined the association of APOE with dementia, its association with cognitive decline over the adult life course remains debated [11, 12]. Some studies show accelerated cognitive decline in APOE ε4 homozygotes but not heterozygotes [13,14,15].


Furthermore, the association between APOE ε4 and cognition is thought to be modified by age; some [16,17,18] but not all studies [19, 20] report better cognitive performance among ε4 carriers at younger ages. The antagonistic pleiotropy hypothesis [21, 22], whereby a gene is thought to have different effects on health during different life stages, is a possible explanation for the age-varying association of APOE ε4 with cognitive performance over the life course [18, 22, 23].


However, much of the research on APOE is based on adults older than 65 years, followed for less than 10 years, making it difficult to ascertain how APOE shapes cognitive performance over the life course.

Link - https://alzres.biomedcentral.com/articles/10.1186/s13195-020-00740-0#Sec2

Combining berberine, quercetin, and piperine (black pepper extract) in a single supplement is relatively uncommon.

However, some formulations include these ingredients to enhance absorption and efficacy.

For instance, Pure Encapsulations offers a supplement called "Curcumin with Bioperine," which contains curcumin and piperine to improve bioavailability.

While this product doesn't include berberine or quercetin, it exemplifies the use of piperine to enhance nutrient absorption. (https://www.health.com/best-joint-supplements-8683190?utm_source=chatgpt.com))

If you're interested in a supplement that combines berberine, quercetin, and piperine, you might consider taking them separately or consulting with a healthcare provider to ensure appropriate dosing and to avoid potential interactions.

It's important to note that while piperine can enhance the absorption of certain compounds, it may also affect the metabolism of various medications, so professional guidance is recommended.

https://www.verywellhealth.com/best-berberine-supplements-8704634

If you are in the your 30-40 years old you should know, that you have about 350,000 hours left, unless you help yourself by investing anything you have (time, efforts, money & etc) into any longevity company or research

Spices for Longevity: Turmeric’s Anti-Aging Properties 🌱

Turmeric, known for its bright yellow color, contains curcumin, a compound with powerful anti-inflammatory and antioxidant effects. Studies suggest that curcumin can help reduce the risk of chronic diseases like heart disease, Alzheimer's, and cancer. Regular consumption of turmeric may contribute to longevity by protecting cells from damage.
Learn more about turmeric’s benefits [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664031/).

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How Green Spaces Impact Longevity 🌳

Living near green spaces, like parks or forests, has been shown to reduce stress, lower blood pressure, and improve mental health. A study from *Environmental Health Perspectives* found that people living close to nature had a lower risk of mortality from chronic diseases. Spending time in green spaces may be a natural way to extend lifespan.
Discover more about the impact of green spaces on longevity [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7851085/).

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Mindfulness for Healthy Aging: Slowing Down the Clock 🧘

Practicing mindfulness has been linked to lower levels of stress and improved emotional well-being. Research shows that mindfulness can reduce inflammation, improve immune function, and even slow cellular aging. A study from *Biobehavioral Medicine* found that mindfulness practices positively influence telomere length, a marker of biological aging.
Read more about mindfulness and aging [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6189422/).

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Fiber-Rich Diet for a Longer Life 🌾

A diet high in fiber, particularly from whole grains, fruits, and vegetables, is linked to lower risks of heart disease, diabetes, and even cancer. Fiber supports digestive health, reduces inflammation, and helps regulate blood sugar. Research from *The Lancet* suggests that people with high fiber intake have a reduced risk of early death.
Learn more about the longevity benefits of fiber [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6647660/).

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How Proper Sleep Hygiene Extends Lifespan 🛌

Quality sleep is crucial for your health and longevity. Studies show that poor sleep is linked to an increased risk of diseases like heart disease and diabetes. Practicing good sleep hygiene—like maintaining a consistent sleep schedule and avoiding screens before bed—can help improve sleep quality and support a longer, healthier life.
Find out more about the link between sleep hygiene and longevity [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449130/).

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Vitamin E: An Antioxidant for Anti-Aging 🥜

Vitamin E is a powerful antioxidant that helps protect cells from oxidative damage, which can accelerate aging. It also supports immune function and skin health. Studies suggest that regular intake of vitamin E through foods like nuts and seeds may slow aging and reduce the risk of chronic diseases.
Discover the benefits of vitamin E for aging well [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7766596/).

Incorporation of photosynthetically active algal chloroplasts in cultured mammalian cells towards photosynthesis in animals
https://www.jstage.jst.go.jp/article/pjab/advpub/0/advpub_pjab.100.035/_article