7th in the series - Alzheimer’s, Social Connectivity and Online Multiplayer Gaming

 

The feeling of caring and lasting relationships, and belonging are fundamental social needs. I came across a remarkable documentary on Netflix titled “ The Remarkable Life of Ibelin”. We all feel that video games are just shooting and violence and only for children. That’s what we saw in video parlors.  When we were growing up, that’s how video games were. But the above video shattered my myth.  The World of Warcraft is a multiplayer game, with social interactions across many people.  Just like in a real world, you can interact with players in different roles and ways and establish friendships.  You can have an avatar that is different, more meaningful, less fearful, more true to yourself.  But just like in real life, you can garner social connections, social wellbeing in the game, or just like in life, can create social isolation and ill being and loneliness.  This does not depend on how many hours you play but how you play.  If you are harmonious and passionate in the game, your character generates social wellbeing but if you are inflexible and passionate in the game, the game would not contribute to your social wellbeing feelings. How remarkable is that!

But here are the implications.  You are bedridden and sick.  Why that makes you sad? Because you are not being useful, socially connected and you don’t matter to anyone, life goes on.  Rather than being sad in bed, why not connect virtually and be who and how you want to be in the virtual world? Your sickness does not matter and you can live a productive life by coming across people and helping them whichever way you can through virtual relationships. Can you do  this by passively watching TV? But that’s what they make you do,  in the hospital or at home.  Yes, maybe you can read a book, listen to music, but that is complete isolation, the only connection is between the author and you.  Again there is no real contribution by you. Given your limitations, you can still be productive in the virtual world or The World of Warcraft, where real people are interacting in avatars, they don’t know you are sick or bedridden.  Imagine the people in old age homes, nursing homes, hospice care, single spouse with mobility challenges, depression and anxiety sufferers, and kids with autism or social phobias.  Given an idle mind is a devil's workshop, why not make it busy with massively multiplayer online role playing games (MMORPG) when you truly cannot get up?. Wouldn’t this benefit Alzheimer’s, and dementia patients? Research proves that.  

Read more on https://mindyourthoughts.org/

6th in the series - Alzheimer’s and Social Connectivity

The remaining lifestyle changes after diet were exercise, emotions, stress, and social connectivity. Let’s tackle social connectivity next.

Oxytocin is one of the key neurotransmitters controlling social behaviors, attachments, and interactions with the stress responses of the HPA axis (which includes the hypothalamus, pituitary gland, and adrenal glands). One very simple example of the power of social bonds is revealed in this clinical trial. One group of HIV-positive, AIDS-symptomatic gay men was allowed to openly discuss both their sexual orientation and their HIV-positive status with others. In contrast, the second group was not permitted to disclose this information. The first group of patients showed a much slower progression of the disease compared to the second group. This study highlighted the healing power of social bonds.

Additionally, in another study, oxytocin levels were measured during group singing versus speaking or singing alone. Group singing enhanced oxytocin levels, signifying stronger social bonding. Another study in a small fishing village in Congo examined the combination of oxytocin and testosterone within a family setting. Fathers who were considered better providers for their families had higher testosterone and lower oxytocin levels compared to those who were poor providers. This pattern was also seen in families with ongoing conflicts. On the other hand, mothers displayed opposite levels when fathers were less involved in caregiving. This suggests that a lot of social connectivity begins at home within the family unit.

A well-known example of this concept is supported by research on telomeres in baboons in Kenya. Aggressive alpha baboons were compared to more social, cooperative, and non-aggressive baboons. The alpha baboons had shorter lifespans, and DNA analysis revealed that they had shorter telomeres-protective caps on the ends of DNA strands - which were linked to their shorter lifespans. This finding correlates with Dr. Hans Selye’s stress research on the paradox of species, balancing self-preservation with social good. Future posts will explore the role of stress in more detail. However, it is important to find a balance between self-preservation and contributing to social good, as an imbalance can lead to the kind of social connectivity stress we are emphasizing here.

It’s important to note that social reward is not solely dependent on one neurotransmitter, such as oxytocin or serotonin. Instead, it results from multiple, parallel mechanisms, making it a complex phenomenon. This means there are many ways to derive social rewards, and it’s worth investing time in discovering what works best for you. These could be connections with various interest groups, reflecting the diversity of interests we have.

Diet and Human Evolution

In this post let’s digress for a minute from Alzheimer's and look at the brain development across evolution of humans.

How Food Scarcity Shaped Human Resilience

During evolution, individuals had to go through periods of no food in the day, or prolonged physical exertion or starvation sometimes.  There was no reliable source of food so starvation was something that they had to get over and survive. The exertion side of this equation, we will address in a different post on the exercise effects.  This resilience throughout their lifespan gave them better bodies and minds to cope with stress.  This metabolic switch to ketones fueling the cells in the neuronal networks in the brain lead to increased resistance to stress, injury and disease.  It also makes sense from this perspective, food is a number one survival intelligence needed for the self, protection from danger being the second which is needed more infrequently compared to food which is on an 8 hour cycle for humans. So food stress definitely has strong implications on brain and intelligence in early humans.  So based on this, an intermittent diet or fasting builds that resistance and repairs inflammation and oxidative stress.  A lot of the signaling is done by Gherlin, the hunger hormone released in gut cells and circulates in blood, acting at the hippocampus. Lab results on mice showed a 40% increase in lifespan for Alzheimer’s with intermittent fasting.

The Evolution of the Human Diet: From Fruit to Seafood, and Beyond

If we look at the diet evolution, apes and chimpanzees ate fruit.  So we started out with a fruit diet, then added meat when we started making hunting tools.  But all of these human-like tribes disappeared and homo sapiens sustained in South Africa where they depended on sea food.  The theory is that the easy to digest sea food with abundant omega-3 oils could have played a role in brain development, as the brain is a massive cell membrane region needing high amounts of fat for the phospholipid layers as language and other faculties improved.  Cooking was used 800,000 years ago so that it allowed a variety of ingredients to become edible for humans, leading to complex diets that our brains demanded. The grain and vegetable diet came on only later when the nomadic lifestyle changed and cultivation started.  Complex traits of language evolved around 100,000 years ago.  Coordinated civilizations occurred 12,000 years ago.  Only the highly adaptable homo-sapiens were able to survive showing that social and stress management is a higher order skill and therefore just diet alone is not sufficient to heal.  In math this is called a necessary but not a sufficient condition.    

Diet and Alzheimer's: The Challenge Isn't Knowledge, It's Implementation

We are concluding in this post the diet part of the lifestyle changes that can lead to reversal of or slow down Alzheimer's progression. The central message is diet knowledge everyone may have, but putting it into daily practice is very difficult and creative psychological solutions are needed, the innovation is in this psychology and not in the diet. One example is why not make salad a compulsory part of food at parties and take away the sweets for once?  Without such large-scale cultural changes, we cannot change our habits.  

Read more on https://mindyourthoughts.org/

Socio Psychological behaviors of diet

 

So far we started out talking about Alzheimer's research results of lifestyle changes reversing the disease, then delved into molecular mechanisms followed by diet discussion. It’s nothing new on diet, we have been told about all this before. The only promising thing is definitive clinical trials are showing lifestyle changes make a difference conclusively.

But it’s not so easy to make a change in lifestyle. So let’s digress a little bit from Alzheimer's biology in this post. We think we can but consistent daily habits have to change. For example, I have replaced coffee with tea with many ingredients that reduce inflammation. But it took me almost a year for it to become my daily habit. It took a lot of tweaking of the tea to make it taste great and feel the difference after I consumed it, and still wakes me up like coffee. The recipe is shared on my website, https://mindyourthoughts.org/. I will be posting recipes to make such replacements on my site. Please check it out from time to time.

Similarly our diets are devoid of good oils and the oils we eat are in the cooking of the foods. But you can put coconut oil or ghee or olive oil in salads, lentils especially are conducive to it, on rice, on roti or bread as you eat your regular food. Again rice, roti, bread can be made with cauliflower instead of processed grains. But this requires a significant attitude change.

Sugars are very damaging as inflammatory agents and creative habits need to be developed to get around them. I used, take a significantly small portion of the item, then completely avoid looking at them, and eat a substitute like betel leaves or antacid tablet, to signal my meal is complete.

Instead of regular milk, I substituted almond, cashew, oat and soy milks. I make the first three at home right before I need them so they taste fresh. Since yogurt is probiotic, I figured out a way to make yogurt out of them also. Again the experimentation took time and taste and consistency took time to develop to my needs.

When I am at dinner parties, I scan the food first, and then stand in line and decide how I am going to combine the food to reach my alternative diet objectives. I found, using curries as dressings for salads and other such creative approaches are needed.

I have come up with substitute behaviors to drinking alcohol like bringing my own coconut water, water melon juice to mix into other non alcoholic drinks from the bar etc.

So bottom line, you have to become creative, persistent and committed to the lifestyle change to make it into a daily routine.

For more info go to https://mindyourthoughts.org/

Understanding the Significance of New Insights in Alzheimer’s Disease

Recent findings in Alzheimer’s research have sparked crucial discussions within the medical community, particularly regarding the role of the brain’s immune response in the progression of the disease. Groundbreaking studies emphasize the complex interplay between inflammation, immune activation, and neurodegeneration, shedding light on new therapeutic avenues.

The Immune System's Role in Alzheimer's Disease

Traditionally, Alzheimer’s disease has been primarily associated with the accumulation of amyloid plaques and tau tangles in the brain. However, recent research highlights the significance of the brain's immune response, particularly the role of microglia—immune cells responsible for maintaining homeostasis in the central nervous system.

Microglia are not just passive responders to neuronal damage; they are active participants in the disease process. When microglia are activated in response to amyloid buildup, they can exhibit a dual nature: they protect neurons by clearing debris and facilitating repair, but they can also contribute to neuronal damage if their activation becomes chronic. This dual role is critical for understanding Alzheimer’s pathology, as chronic activation of microglia leads to sustained inflammation and further neuronal injury.

Implications of Chronic Inflammation

Chronic inflammation driven by an overactive immune response can lead to a cascade of events detrimental to neuronal integrity. Prolonged microglial activation releases pro-inflammatory cytokines, exacerbating neuroinflammation and contributing to neuronal cell death. This vicious cycle accelerates cognitive decline and worsens symptoms.

Research published in journals like Nature Reviews Neuroscience and The Journal of Neuroscience confirms that chronic microglial activation correlates with increased neuroinflammation and cognitive impairment in animal models. This understanding not only sheds light on how Alzheimer’s develops but also raises critical questions about intervention points. Could modulating the inflammatory response halt or even reverse some of the damage caused by the disease?

A recent study from Alzheimer’s Research & Therapy further emphasizes this point, revealing that specific inflammatory markers, such as cytokines and chemokines, are significantly elevated in the brains of Alzheimer’s patients. The study indicates that targeting these markers may provide new strategies for intervention, suggesting that modulating the immune response could help restore balance and reduce neurodegeneration.

Novel Therapeutic Strategies

The insights from these studies suggest promising new therapeutic strategies. Targeting the inflammatory pathways associated with microglial activation may yield novel interventions that address not only amyloid and tau but also modulate the immune response to promote brain health.

For instance, research published in Frontiers in Neuroscience discusses pharmacological agents that inhibit overactive microglial activation without completely shutting down their function. This approach preserves their ability to clear amyloid plaques while mitigating harmful effects on neurons. Additionally, repurposing anti-inflammatory agents already used for other conditions could provide new avenues for Alzheimer’s treatment. A study in Alzheimer's & Dementia highlighted that nonsteroidal anti-inflammatory drugs (NSAIDs) might have protective effects against cognitive decline.

A Paradigm Shift in Understanding Alzheimer’s

The implications of these findings challenge the long-standing notion that Alzheimer’s is solely a result of toxic protein accumulation. Instead, they encourage a holistic view that includes the brain’s immune landscape.

Recognizing neuroinflammation's significance opens new avenues for research and improved diagnostic tools. For instance, measuring inflammatory markers in cerebrospinal fluid or utilizing advanced imaging techniques to visualize microglial activation could allow for earlier, more accurate diagnoses.

A compelling study published in Neurobiology of Disease suggests that inflammatory biomarkers could help identify individuals at high risk for developing Alzheimer’s, facilitating timely interventions to slow disease progression. Furthermore, the recent findings in the Alzheimer’s Research & Therapy study indicate that monitoring changes in these inflammatory markers could also serve as a potential measure of treatment efficacy, allowing for more personalized therapeutic approaches.

Future Directions in Research

Exploring the relationship between inflammation and neurodegeneration reveals several key research directions. Longitudinal studies examining microglial activation timing and extent in relation to cognitive decline could clarify causal relationships. Understanding whether early intervention in inflammatory pathways can prevent or delay Alzheimer’s symptoms is critical.

Additionally, investigating genetic and environmental factors that influence microglial behavior may provide insights into individual susceptibility. Research in Nature Genetics has highlighted genetic variants affecting microglial function, suggesting these factors may influence an individual’s Alzheimer’s risk and treatment response.

Conclusion

In conclusion, the findings from recent studies illuminate the critical role of the immune system in Alzheimer’s disease, highlighting the potential for innovative therapeutic strategies. By deepening our understanding of the interplay between inflammation and neurodegeneration, we move closer to comprehensive approaches that could ultimately change the course of this devastating disease.

Embracing these insights will be key to advancing research and clinical practice in the fight against Alzheimer’s. A collaborative effort among researchers, clinicians, and policymakers is essential to ensure that the lessons learned from these studies translate into effective treatments and improved outcomes for individuals affected by Alzheimer’s disease. As we continue to unravel the complexities of this condition, the hope for more effective interventions becomes increasingly tangible.

For more info go to https://mindyourthoughts.org/