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ADHD Clinic in Arlington, 1833 W Pioneer Pkwy, Arlington, TX (2025)

03/22/2024

The Links between Autophagy and Longevity: Does autophagy reverse aging?
Autophagy, as the key nutrient recycling pathway, enables eukaryotic cells to adapt to surging cellular stress during aging and, thereby, delays age-associated deterioration. Autophagic flux declines with age and, in turn, decreases in autophagy contribute to the aging process itself and promote senescence.

With the global increase in life expectancy, understanding the biological mechanisms that promote healthy aging is of paramount importance. Autophagy, a cellular degradation pathway, has emerged as a crucial player in the longevity equation. This review delves into the current body of research exploring the connection between autophagy and longevity, with a particular focus on how autophagy influences age-related diseases and the aging process itself. Ultimately, this understanding could inform therapeutic strategies to promote health in old age and extend human lifespan. Introduction: Autophagy is a cellular process that serves to degrade and recycle damaged organelic and protein aggregates, thereby maintaining cellular homeostasis. Accumulating evidence points to the role of autophagy in promoting longevity, with implications for various age-related diseases including neurodegenerative disorders, cancer, and cardiovascular diseases.
Recent findings on the role of autophagy in aging and longevity, including its effects on cellular senescence, immune response, and metabolic regulation. There is potential therapeutic applications, such as the use of autophagy inducers and inhibitors to modulate lifespan and healthspan. Understanding the intricate relationship between autophagy and longevity may pave the way for innovative therapeutic strategies to combat aging and age-related diseases. Further research is needed to unravel the complex regulatory networks of autophagy and to develop safe and effective interventions that can harness the power of autophagy for human health and longevity.
Starvation-induced autophagy was proven to be causal to lifespan extension in several animal models from yeasts to great apes (65, 66). Moreover, direct inhibition with rapamycin of the mTOR kinase, a master nutrient-sensing regulator of autophagy, systematically increased the median and maximum lifespan of mice.
Does autophagy increase survival?
Autophagy promotes cell survival by catabolism of intracellular resources to maintain bioenergetics under nutrient limiting conditions. Furthermore, the elimination of damaged organelles and toxic protein aggregates by autophagy promotes cell survival.
Four well-studied pathways that are known to regulate aging, and whose modulation has been shown to influence the rate of aging are Insulin/IGF-1, mechanistic target of rapamycin (mTOR), AMP-activating protein kinase (AMPK), and Sirtuin pathways.
Does autophagy heal everything?
An increasing number of studies show that autophagy is particularly essential for wound healing and repair; however, our current understanding of the systematic relationship between wound healing and autophagy is insufficient.F

How many times a year should you fast for autophagy?
Autophagy fasting can be something you invest in through small, consistent fasts lasting 17 or more hours, or you can opt to do longer fasts less frequently; perhaps a few times each year, you do a 48–72 hour fast to maximize your fasting autophagy.

What lifestyle promotes longevity?
But with common sense, healthy habits such as regular exercise, a healthy weight, avoiding red meat, not smoking, and managing stress, it can be 'the older you get, the healthier you've been,'” Perls says. The key to healthy aging is to engage fully in life—mentally, physically, and socially.
What are the 9 secrets to longevity?
Many residents living in the original Blue Zones® areas share nine healthy lifestyle habits that help them live longer, healthier lives.
• MOVE NATURALLY. The world's longest-lived people don't pump iron, run marathons or join gyms. ...
• KNOW YOUR PURPOSE. ...
• DOWN SHIFT. ...
• 80% RULE. ...
• PLANT SLANT. ...
• FRIENDS @ FIVE. ...
• POSITIVE PACK. ...
• BELONG.
Autophagy is an evolutionally conserved cytoplasmic degradation system in which varieties of materials are sequestered by a double membrane structure, autophagosome, and delivered to the lysosomes for the degradation. Due to the wide varieties of targets, autophagic activity is essential for cellular homeostasis. Recent genetic evidence indicates that autophagy has a crucial role in the regulation of animal lifespan. Basal level of autophagic activity is elevated in many longevity paradigms and the activity is required for lifespan extension. In most cases, genes involved in autophagy and lysosomal function are induced by several transcription factors including HLH-30/TFEB, PHA-4/FOXA and MML-1/Mondo in long-lived animals. Pharmacological treatments have been shown to extend lifespan through activation of autophagy, indicating autophagy could be a potential and promising target to modulate animal lifespan. Here we summarize recent progress regarding the role of autophagy in lifespan regulation.
Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

03/20/2024

MIND DIET HAS A REDUCTION IN RISK OF DEVELOPING ALZHEIMER'S DISEASE BY AS MUCH AS 53%.
Researchers found a 53% lower rate of Alzheimer's disease for those with the highest MIND diet scores (indicating a higher intake of foods on the MIND diet). Even those participants who had moderate MIND diet scores showed a 35% lower rate compared with those with the lowest MIND scores. MIND diet has a reduction in risk of developing Alzheimer's disease by as much as 53%. An analysis of diet and other factors found that, after an average of 4.5 years, people who adhered most closely to the MIND diet had a 53% reduced rate of Alzheimer's compared to those who did not follow the diet closely. The MIND diet, or Mediterranean-DASH Diet Intervention for Neurodegenerative Delay, is a diet that emphasizes foods and nutrients that work to protect the brain. Recent studies have demonstrated that adherence to the MIND diet could potentially reduce the risk of developing Alzheimer's disease by as much as 53%. This dietary approach encourages the consumption of brain-healthy food groups like whole grains, vegetables, berries, nuts, olive oil, and fish. Simultaneously, it discourages foods from five unhealthy groups: red meats, butter and stick margarine, cheese, pastries and sweets, and fried or fast food. The potential for a diet-based approach to significantly reduce the risk of neurodegenerative disease could have profound implications for patient healthcare strategies and public health in general. It may be beneficial to consider these findings when advising patients on lifestyle modifications for disease prevention.
Healthy eating patterns have been associated with cognitive benefits in studies, but more research is needed — and is underway — to determine if what we eat can prevent or delay Alzheimer’s or age-related cognitive decline.
How could what we eat affect our brains? It’s possible that eating a certain diet affects biological mechanisms, such as oxidative stress and inflammation, that underlie Alzheimer’s. Eating a certain diet might increase specific nutrients that may protect the brain through anti-inflammatory and antioxidant properties. It may inhibit beta-amyloid deposits, which are found in the brains of people with Alzheimer’s, or improve cellular metabolism in ways that protect against the disease.Or perhaps a person’s diet works indirectly by affecting other Alzheimer’s risk factors, such as diabetes, obesity, and heart disease. For example, the typical Western diet increases cardiovascular disease risk, possibly contributing to faster brain aging. A growing area of research focuses on the relationship between gut microbes — tiny organisms in the digestive system — and aging-related processes that lead to Alzheimer’s. The important role of physical activity and exercise, and how this interacts with diet, cardiovascular health, and brain health must also be considered.
Understanding the Mediterranean and MIND diets
Before starting any dietary change, it’s important to talk with your health care provider. They can provide personalized advice that accounts for your health history and medical conditions.With that in mind, there are two diets that research has shown may hold potential benefits for cognitive health, but the evidence is mixed.
• The Mediterranean diet emphasizes fruits, vegetables, whole grains, legumes, fish and other seafood, unsaturated fats such as olive oils, and low amounts of red meat, eggs, and sweets.
• The MIND (Mediterranean–DASH Intervention for Neurodegenerative Delay) diet is a hybrid of the Mediterranean and the DASH (Dietary Approaches to Stop Hypertension) diet. Several studies have shown that treating and reducing high blood pressure may help reduce the risk of dementia. Similar to the Mediterranean diet, the MIND diet features vegetables, especially green leafy vegetables; berries over other fruit; whole grains; beans; nuts; one or more weekly servings of fish; and olive oil. It also limits servings of red meat, sweets, cheese, butter/margarine, and fast/fried food.
Some, but not all observational studies have shown that the Mediterranean and MIND diets are associated with a lower risk for dementia compared to a Western-style diet, which typically contains more red meat, saturated fats, and sugar.
However, a recent clinical trial assigned 600 older adults with a family history of dementia to either a MIND-diet group or a control-diet group. Results showed that participants who followed the MIND diet had only small improvements in cognition that were similar to those who followed a control diet of mild caloric restriction.
Previous research on these diets points to their potential to slow cognitive decline, lower risk for dementia, and reduce related damage to the brain. Here’s a look at the evidence:
To find out more on the diet and dementia connection, scientists continue to conduct clinical trials to shed more light on any cause and effect. (View a list of trials currently recruiting participants at the end of this article.)
• Observational studies of more than 900 dementia-free older adults found that closely following the MIND diet was associated with a reduced risk of Alzheimer’s and a slower rate of cognitive decline.
o In March 2023, scientists completed a study of the brains of about 600 older adults who died at an average age of 91. Brain autopsies found that people who had reported sticking to a Mediterranean or MIND diet showed less evidence of Alzheimer’s pathologies, including tau tangles and amyloid plaques.
o In one observational study of 116 cognitively normal adults, those who followed a Mediterranean diet had thicker cortical brain regions than those who did not. These brain regions shrink in people with Alzheimer’s, so having thicker regions could mean there’s a cognitive benefit.
o A follow-up observational study showed lower glucose metabolism and higher levels of beta-amyloid protein — both seen in Alzheimer’s — in people who did not follow the Mediterranean diet closely, compared to those who did.
o An analysis of diet and other factors found that, after an average of 4.5 years, people who adhered most closely to the MIND diet had a 53% reduced rate of Alzheimer’s compared to those who did not follow the diet closely.
o In a similar study, following the MIND diet was associated with a substantial slowing of cognitive decline during an average of almost five years.
o The Age-Related Eye Disease Studies originally looked at diet and eye disease. Further analysis by the researchers showed that people who followed the Mediterranean-style diet had a lower risk of developing cognitive problems while maintaining a higher level of cognitive function. The Mediterranean-DASH Diet Intervention for Neurodegenerative Delay, or MIND diet, targets the health of the aging brain. Dementia is the sixth leading cause of death in the United States, driving many people to search for ways to prevent cognitive decline.
The healthy items the MIND diet guidelines* suggest include:
• 3+ servings a day of whole grains
• 1+ servings a day of vegetables (other than green leafy)
• 6+ servings a week of green leafy vegetables
• 5+ servings a week of nuts
• 4+ meals a week of beans
• 2+ servings a week of berries
• 2+ meals a week of poultry
• 1+ meals a week of fish
• Mainly olive oil if added fat is used
The unhealthy items, which are higher in saturated and trans fat, include:
• Less than 5 servings a week of pastries and sweets
• Less than 4 servings a week of red meat (including beef, pork, lamb, and products made from these meats)
• Less than one serving a week of cheese and fried foods
• Less than 1 tablespoon a day of butter/stick margarine
Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

03/20/2024

Spermidine is an endogenously synthesized and nutritional metabolite that is positively correlated with longevity. Spermidine functions as an antioxidant and promotes autophagy. Whole blood spermidine concentrations decline with age in most animals and humans but are higher than expected in humans of advanced age and increase with age in the exceptionally long-lived naked mole rat. Previous studies have established the role of spermidine in longevity; here, we report its heritability and relationship to other heritable metabolites and proteins that appear to be linked to longevity.
Spermidine, a type of polyamine compound found in ribosomes and living tissues, has been linked to various health benefits, including potentially promoting longevity. Research has suggested that spermidine may have the ability to induce autophagy, a cellular process that recycles and removes unnecessary or dysfunctional components. This process is essential for cellular rejuvenation and proper functioning. Dysregulation of autophagy is associated with various diseases, including neurodegenerative disorders, infections, and cancers. Studies in yeast, flies, worms, and human immune cells have indicated that spermidine can extend lifespan. Some research in mice has also suggested that dietary supplementation with spermidine can enhance cardiac function and reduce hypertension, potentially contributing to increased longevity. In humans, an observational study has shown that increased dietary intake of spermidine is associated with reduced blood pressure and lower risk of cardiovascular disease, which may contribute to increased longevity. However, while these findings are promising, more research is needed to fully understand the potential health benefits and risks of spermidine supplementation in humans, including its effects on longevity. Always consult with a healthcare professional before beginning any new supplement regimen. External supply of the natural polyamine spermidine can extend life span in model organisms including yeast, nematodes, flies and mice. Recent epidemiological evidence suggests that increased uptake of spermidine with food also reduces overall, cardiovascular and cancer-related mortality in humans. Here, we discuss the possible mechanisms of this intriguing spermidine effect. Polyamines including spermidine play an essential role in intermediate metabolism. Since they are synthesized by higher eukaryotic cells, they are not vitamins. However, the levels of polyamines are profoundly influenced by their external supply, either by oral ingestion with different food items or by the intestinal microbiota that can synthesize polyamines as well. Spermidine has been shown to induce autophagy in multiple organs, including liver, heart, and muscle in mice [28], as well as in aging, worms, flies, and cultured mammalian cells.
Spermidine dietary supplementation and polyamines level in reference to survival and lifespan of honey bees: Honey bee health has been an important and ongoing topic in recent years. Honey bee is also an important model organism for aging studies. Polyamines, putrescine, spermidine and spermine, are ubiquitous polycations, involved in a wide range of cellular processes such as cell growth, gene regulation, immunity, and regulation of lifespan. Spermidine, named longevity elixir, has been most analysed in the context of aging. One of the several proposed mechanisms behind spermidine actions is antioxidative activity. In study showed that dietary spermidine supplementation: (a) improved survival, (b) increased the average lifespan, (c) influenced the content of endogenous polyamines by increasing the level of putrescine and spermidine and decreasing the level of spermine, (d) reduced oxidative stress (MDA level), (e) increased the antioxidant capacity of the organism (FRAP), (f) increased relative gene expression of five genes involved in polyamine metabolism, and (g) upregulated vitellogenin gene in honey bees.

Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

03/19/2024

FOOD THAT PRESERVES YOUR TELOMERE LENGTH:
1. Whole Grains: Foods like oats, brown rice, and whole grain bread are high in fiber and have been associated with longer telomeres.
2. Fruits and Vegetables: High in antioxidants and nutrients, fruits and vegetables like berries, leafy greens, tomatoes, and bell peppers can help protect and lengthen telomeres.
3. Omega-3 Fatty Acids: Foods rich in omega-3 fatty acids such as salmon, tuna, flaxseeds, and walnuts have been shown to have a positive effect on telomere length.
4. Nuts and Seeds: Almonds, chia seeds, flaxseeds, and walnuts are not only high in fiber and protein, but also contain nutrients that may help maintain telomere length.
5. Legumes: Beans, lentils, and peas are high in fiber, protein, and a variety of nutrients that are beneficial for telomere health.
6. Green Tea: The antioxidants found in green tea may help protect telomeres from damage and slow the rate of telomere shortening.
7. Tofu and Soy Products: These foods are high in polyphenols, a type of antioxidant that may help preserve telomere length.
8. Dark Chocolate: The antioxidants in dark chocolate may help preserve the length of telomeres.
9. Dairy: Some studies suggest that moderate consumption of dairy products may help maintain telomere length.
10. Avocados: High in healthy fats and fiber, avocados may have a positive impact on telomere length.
Please note that while these foods have been associated with longer telomeres, more research is needed to fully understand the relationship between diet and telomere length. It's also important to maintain a balanced and diverse diet, as well as other healthy lifestyle habits like regular exercise and stress management for optimal health.
Consumption of Specific Foods. Telomere length is positively associated with the consumption of legumes, nuts, seaweed, fruits, and 100% fruit juice, dairy products, and coffee, whereas it is inversely associated with consumption of alcohol, red meat, or processed meat. To preserve telomeres and reduce cancer risk and pace of aging, we may consider to eat less; include antioxidants, fiber, soy protein and healthy fats (derived from avocados, fish, and nuts) in our diet; and stay lean, active, healthy, and stress-free through regular exercise and meditation. Dietary restriction, appropriate diet (high fiber, plenty of antioxidants, lean/low protein, adding soy protein to diet), and regular exercise can potentially reduce the rate of telomere shortening, disease risk, and pace of aging. Most studies indicate an important role of diet on the degree of biological aging. Indeed, a healthy diet characterized by a high intake of dietary fiber and unsaturated lipids exerts a protective role on telomere health, whereas high consumption of sugar and saturated lipids accelerates telomere attrition. With each cell replication, the telomeres get shorter and shorter until they're so short that your cells can no longer divide. When cells no longer divide, tissues age. However, telomeres can be rebuilt by an enzyme called telomerase to restore cell division.
CAN YOU REGROW TELOMERES?
When telomeres become too short to function effectively, a cell either dies or stops dividing. So because most cells cannot regenerate their telomeres, they become shorter as people age. The rate at which telomeres shorten has also been associated with rates of aging.
Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

03/19/2024

Telomere length shortening is a natural part of aging, but research suggests that certain lifestyle modifications may help slow this process.
Here are some recommendations:
1. Healthy Diet: Consuming a diet rich in fruits, vegetables, lean proteins, and whole grains can provide the body with the necessary nutrients for maintaining cellular health, including telomeres.
2. Exercise: Regular physical activity has been associated with longer telomeres. The precise amount and type of exercise can vary, but generally, a mix of cardiovascular exercises, strength training, and flexibility exercises is recommended.
3. Stress Management: Chronic stress has been linked to shorter telomeres. Therefore, engaging in stress-reducing activities such as meditation, yoga, breathing exercises, or other relaxation techniques can be beneficial.
4. ADEQUATE SLEEP: QUALITY SLEEP IS ESSENTIAL FOR OVERALL HEALTH AND MAY ALSO PLAY A ROLE IN MAINTAINING TELOMERE LENGTH. AIM FOR 7-9 HOURS OF SLEEP PER NIGHT.
5. Limit Alcohol and Avoid Smoking: Both excessive alcohol and smoking have been associated with shorter telomere length. Thus, limiting alcohol intake and avoiding smoking can contribute to telomere health.
6. MAINTAIN A HEALTHY WEIGHT: OBESITY HAS BEEN LINKED TO SHORTER TELOMERES. THEREFORE, MAINTAINING A HEALTHY WEIGHT THROUGH A BALANCED DIET AND REGULAR EXERCISE CAN HELP PRESERVE TELOMERE LENGTH.
7. ANTIOXIDANTS AND OMEGA-3 FATTY ACIDS: THESE ARE KNOWN TO REDUCE INFLAMMATION AND OXIDATIVE STRESS, WHICH MAY HELP SLOW DOWN TELOMERE SHORTENING.

Remember, it's always important to consult with a healthcare provider before starting any new health regimen.
Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

03/19/2024

Yes, there is a link between telomere length shortening and the risk of cancer. Telomeres are the protective caps at the end of chromosomes that shorten with each cell division. When they become too short, the cell can no longer divide and becomes senescent or dies, which is a normal part of aging. However, in some cases, instead of entering senescence, these cells can become "immortal" and continue dividing, leading to uncontrolled cell growth, a hallmark of cancer. Thus, shortened telomeres can lead to genomic instability, promoting the development of cancer. Several studies have shown an association between shorter telomeres and increased risk of various types of cancer, including lung, breast, ovarian, and colorectal cancer. However, the relationship between telomere length and cancer is complex, as some studies have also found that longer telomeres can increase the risk of certain other cancers, such as melanoma.

Are Telomeres the Key to Aging and Cancer???
Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.
Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism's genetic information.
Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or "senescent" or it dies. THIS SHORTENING PROCESS IS ASSOCIATED WITH AGING, CANCER, AND A HIGHER RISK OF DEATH.

More research is needed to fully understand the complex relationship between telomere length and cancer risk and to develop potential therapeutic strategies targeting telomeres in cancer.

Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

03/19/2024

Telomeres are at the non-coding ends of linear chromosomes. Through a complex 3-dimensional structure, they protect the coding DNA and ensure appropriate separation of chromosomes. AGING IS CHARACTERIZED BY A PROGRESSIVE SHORTENING OF TELOMERES, WHICH COMPROMISES THEIR STRUCTURE AND FUNCTION. Because of their protective function for genomic DNA, telomeres appear to play an important role in the development and progression of many age-related diseases, such as cardiovascular disease (CVD), malignancies, dementia, and osteoporosis. Despite substantial evidence that links telomere length with these conditions, the nature of these observations remains insufficiently understood. Therefore, future studies should address the question of causality.
TELOMERE LENGTH SHORTENS WITH AGE. PROGRESSIVE SHORTENING OF TELOMERES LEADS TO SENESCENCE, APOPTOSIS, OR ONCOGENIC TRANSFORMATION OF SOMATIC CELLS, AFFECTING THE HEALTH AND LIFESPAN OF AN INDIVIDUAL. SHORTER TELOMERES HAVE BEEN ASSOCIATED WITH INCREASED INCIDENCE OF DISEASES AND POOR SURVIVAL.

Exploring the Correlation between Telomere Length, Longevity, and Dementia Abstract: Telomeres, the protective caps at the end of chromosomes, are recognized as critical components in the mechanisms of cellular aging and disease progression. Their length is often considered as a biological marker for aging, longevity, and diseases associated with aging like dementia. The complex relationships between telomere length, longevity, and the onset and progression of dementia.
Telomeres are repetitive DNA sequences at the ends of chromosomes that protect them from degradation or fusion with neighboring chromosomes. Each time a cell divides, its telomeres shorten, and once they reach a critical length, the cell enters senescence or programmed cell death. This process is believed to play a significant role in human aging and longevity. Concurrently, diseases associated with aging, such as dementia, have been linked to telomere length. However, the relationship between telomere length, longevity, and dementia is complex and not fully understood.
Multitude of studies, drawing from epidemiological data, genetic studies, and cell biology research. It will also consider potential confounding factors such as lifestyle and environmental influences on telomere length.
The relationship between telomere length and longevity is not straightforward, with both longer and shorter telomere lengths associated with different health outcomes. Similarly, the role of telomere length in dementia is complex, with some studies suggesting shorter telomeres may contribute to the onset and progression of the disease, while others show no significant association.
The relationships between telomere length, longevity, and dementia are intricate and multifaceted. More research is required to fully understand these relationships and their potential implications for disease prevention and treatment strategies. Understanding these relationships could lead to novel therapeutic approaches to extend healthy lifespan and mitigate age-related diseases like dementia.

Telomere length shortens with age. Progressive shortening of telomeres leads to senescence, apoptosis, or oncogenic transformation of somatic cells, affecting the health and lifespan of an individual. Shorter telomeres have been associated with increased incidence of diseases and poor survival. The rate of telomere shortening can be either increased or decreased by specific lifestyle factors. Better choice of diet and activities has great potential to reduce the rate of telomere shortening or at least prevent excessive telomere attrition, leading to delayed onset of age-associated diseases and increased lifespan. This review highlights the role of telomeres in aging and describes the lifestyle factors which may affect telomeres, human health, and aging.
Telomere theory depends on three specific principles, the three pillars the Telomere theory stands on: first, that aging is programmed; the second being that irreversible cell cycle arrest happens in response to the telomere shortening; and lastly, that the total number of cell divisions in the absence of telomerase ..
Please visit my telepsychiatry virtual waiting room. https://doxy.me/drquaziimam
Quazi Imam, M.D. Board Certified in Psychiatry. Board Certified in Addiction Psychiatry. Board Certified in Geriatric Psychiatry. Board Certified in Forensic Psychiatry. Former Assistant Professor of Psychiatry, Mount Sinai School of Medicine, NY. Child & Adolescent Psychiatrist, Harvard Medical School Trained.

ADHD Clinic in Arlington

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