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Millions of Americans are turning to weight-loss medications such as Ozempic, Wegovy, Mounjaro, and Zepbound. And while many are celebrating losing 20, 40, 60, or even 100 pounds, I believe an important conversation is being overlooked.

What happens to the brain when someone consistently eats so little food that they’re no longer meeting their essential nutritional needs?

My concern is not that glucagon-like peptide-1 (GLP-1) medications have been proven to directly damage the brain. They haven’t.

My concern involves something more fundamental: human physiology.

These medications help people lose weight largely by suppressing appetite, increasing feelings of fullness, and reducing food consumption. This creates the calorie deficit responsible for much of the weight loss.

But healthy weight loss isn’t about eating as little as possible.

It’s about consuming fewer calories than your body expends while continuing to meet your nutritional requirements.

That means adequate protein, essential amino acids, vitamins, minerals, essential fatty acids, dietary fiber, and an appropriate intake of carbohydrates.

And that’s where I believe we have a serious problem when patients receive weight-loss prescriptions without comprehensive nutritional guidance.

A person can lose a significant amount of weight while simultaneously becoming nutritionally compromised.

This is particularly concerning for adults age 65 and older, who may already be experiencing age-related muscle loss and increased vulnerability to cognitive decline.

Research has established that severe nutritional deprivation can affect brain structure, including measurable reductions in brain volume. Certain patterns of brain atrophy are also associated with dementia and Alzheimer’s disease.

These findings do not establish that GLP-1 medications cause Alzheimer’s disease. However, they raise an important question: Could inadequate nutrition during prolonged medication-assisted weight loss compromise brain health, particularly among older adults?

I believe this deserves serious scientific attention.

Your Brain Requires an Extraordinary Amount of Energy

Let’s begin with something most people don’t realize.

Your brain represents approximately 2% of your body weight, yet it accounts for roughly 20% of your body’s resting energy expenditure [1].

Think about that.

If your body uses approximately 2,000 calories daily at rest, your brain may account for roughly 400 of those calories.

Why?

Because your brain never stops working.

Even while you’re sleeping, billions of neurons are maintaining electrical activity, communicating with one another, regulating essential bodily functions, and supporting cellular maintenance.

These processes require adenosine triphosphate (ATP), the primary energy currency used by our cells.

The brain has limited local energy reserves and depends on a continuous supply of metabolic fuel.

However, here’s an important distinction.

A calorie deficit does not automatically mean your brain is being deprived of energy.

When you consume fewer calories than your body burns, your body can draw on stored energy.

The liver helps maintain blood glucose through glycogen breakdown and glucose production. During prolonged fasting or carbohydrate restriction, the brain can also increase its use of ketone bodies [2].

These are normal physiological adaptations.

But here’s where the problem can begin.

Your body can draw on stored fat for energy, but stored fat cannot replace all the essential nutrients required for healthy brain function.

The body cannot manufacture every essential amino acid, essential fatty acid, vitamin, or mineral it needs.

Therefore, someone can have ample stored body fat while experiencing nutritional deficiencies.

And those deficiencies can affect the nervous system.

GLP-1 Medications Work Primarily by Helping People Eat Less

GLP-1 is a naturally occurring hormone involved in appetite regulation, digestion, and blood glucose control.

Medications such as semaglutide, the active ingredient in Ozempic and Wegovy, activate GLP-1 receptors.

Tirzepatide, found in Mounjaro and Zepbound, activates both GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) receptors.

These medications influence appetite-related signaling, increase fullness, and help people feel satisfied after consuming less food.

As a result, many people substantially reduce their daily calorie intake.

Research reviewed in The Journal of Nutrition indicates that GLP-1 treatment can produce substantial reductions in voluntary energy intake, although the amount varies considerably between individuals [3].

This is a major reason people lose weight.

But there is a physiological distinction between eating less and eating too little.

Consider two people.

One reduces daily calorie intake from 3,000 to 2,200 calories while consuming balanced meals containing adequate protein, vegetables, fruit, essential fats, and other nutrient-rich foods.

The other reduces intake from 3,000 to 900 calories because appetite suppression makes eating difficult.

Both may lose weight.

But the second person faces a greater challenge meeting essential nutritional requirement.

The calorie deficit itself is not necessarily the problem.

The concern is whether the amount and quality of food consumed are sufficient to maintain healthy tissues, including skeletal muscle and the brain.

Healthy Weight Loss Is Not About Eating as Little as Possible

For more than three decades, I’ve educated people about the difference between losing weight and improving metabolic health.

And one of the biggest mistakes people make is assuming that eating less always means becoming healthier.

It doesn’t.

Healthy weight loss should involve reducing excess body fat while preserving muscle, maintaining adequate nutrition, and improving physical function.

That requires attention to several nutritional priorities.

Protein and essential amino acids: Protein supplies the building blocks required for maintaining skeletal muscle, repairing tissues, producing enzymes, and synthesizing neurotransmitters.

Vitamins: Nutrients such as thiamine (vitamin B1), vitamin B12, and folate support neurological function and cellular metabolism.

Minerals: Iron, magnesium, zinc, and other minerals participate in oxygen transport, nerve signaling, and essential metabolic processes.

Essential fatty acids: These support cellular membranes and normal physiological signaling, including processes important to the nervous system.

Dietary fiber: Fiber supports gastrointestinal function, the gut microbiome, and metabolic health.

Carbohydrates: Carbohydrates provide an important dietary energy source. Although the body can manufacture glucose and use ketones during carbohydrate restriction, carbohydrate intake should be individualized to support nutritional adequacy, metabolic health, and activity needs.

This is why I believe simply telling someone to eat less is inadequate nutritional guidance.

A weight-loss plan should help someone eat appropriately—not merely eat as little as possible.

When Appetite Suppression Creates a Risk of Malnutrition

One of the biggest misconceptions about malnutrition is that it only affects people who are extremely thin.

That’s not true.

Someone can be overweight or obese and still have significant nutritional deficiencies.

Having excess stored body fat does not guarantee adequate protein, vitamins, minerals, or essential fatty acids.

A 2026 review in The Journal of Nutrition, titled Avoiding Malnutrition in the Era of Glucagon-Like Peptide-1 Medications, emphasized the importance of integrating nutritional assessment and monitoring into GLP-1 treatment [3].

The authors discussed potential problems involving insufficient protein, micronutrients, fiber, and fluids.

They also emphasized evaluating body composition and muscle function rather than relying exclusively on body weight.

Another 2026 review examined hidden malnutrition during GLP-1 therapy and concluded that nutritional responses vary between individuals, with particular concerns for older adults, people with sarcopenic obesity, and those experiencing persistent gastrointestinal symptoms [4].

These findings reinforce an important distinction.

Not everyone taking GLP-1 medications becomes malnourished. But significant appetite suppression can make nutritional inadequacy more likely in vulnerable individuals.

And if nobody is assessing what the person actually eats, nutritional problems may go unnoticed.

Are Healthcare Professionals Doing Enough to Protect Patients?

This is where I believe the medical community needs to examine its approach to GLP-1 prescribing.

I’m not opposed to medications that help people manage obesity or type 2 diabetes.

These medications can provide meaningful benefits, including improved glucose regulation and reduced cardiovascular risk in appropriate patients.

But I am concerned about treatment that places too much emphasis on pounds lost and too little emphasis on nutritional adequacy.

Prescribing a medication that substantially suppresses appetite without appropriately assessing nutritional intake, muscle preservation, and the patient’s overall health represents a serious gap in comprehensive care.

This isn’t simply my opinion about what ideal care should look like.

A joint advisory developed by the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association, and The Obesity Society emphasizes the importance of nutritional assessment, dietary quality, adequate protein, resistance exercise, and monitoring muscle health during GLP-1 treatment [5].

That advisory also acknowledges that substantial weight loss can involve reductions in lean mass.

Importantly, this isn’t unique to GLP-1 medications. Significant weight loss from dietary restriction or bariatric surgery can also involve lean-tissue loss.

But the fact that a complication isn’t unique to a medication doesn’t make it unimportant.

I believe every patient should have access to appropriate nutritional guidance and monitoring—not just a prescription and a scale.

And this responsibility becomes particularly important when treating older adults.

Scientific Research Shows Severe Malnutrition Can Reduce Brain Volume

Now let’s examine one of the most important biological findings in this discussion.

Severe nutritional deprivation can be associated with measurable reductions in brain volume.

A 2026 meta-analysis published in NeuroImage: Clinical examined structural brain changes in individuals with anorexia nervosa, a condition frequently involving severe undernutrition [6].

The researchers analyzed findings from 40 papers involving 1,130 patients.

Among individuals experiencing acute anorexia nervosa, researchers reported:

• • Gray matter volume approximately 4.79% lower.
  • White matter volume approximately 2.48% lower.
  • Cerebrospinal fluid volume approximately 17.11% higher.

These findings deserve attention.

Gray matter contains many of the brain’s neuronal cell bodies and is involved in processing information.

White matter contains nerve fibers that help different brain regions communicate.

Cerebrospinal fluid surrounds and protects the brain and spinal cord.

When brain tissue volume decreases, the spaces occupied by cerebrospinal fluid may increase.

Interestingly, the researchers also found that brain volumes generally improved with nutritional rehabilitation, although some differences persisted after recovery.

This demonstrates an important biological principle.

The brain’s physical structure can be affected by severe nutritional deprivation, and some of those changes may improve when adequate nutrition is restored.

However, we need to make an important distinction.

Anorexia nervosa is a complex medical and psychiatric condition that can involve extreme undernutrition, hormonal disturbances, and other physiological complications.

These findings cannot automatically be applied to someone taking a GLP-1 medication while maintaining a nutritionally adequate calorie deficit.

The research does not establish that ordinary medication-assisted weight loss causes equivalent brain shrinkage.

What it does establish is that severe undernutrition can affect brain structure.

And that makes nutritional adequacy during prolonged appetite suppression a legitimate subject for investigation.

Brain Shrinkage and Alzheimer’s Disease Are Not the Same Thing

Alzheimer’s disease is the most common cause of dementia.

It involves progressive neurological changes that interfere with memory, thinking, and everyday functioning.

One characteristic of Alzheimer’s disease is the loss of neurons and connections between brain cells.

Over time, certain brain regions may shrink.

This process is called brain atrophy.

One particularly important region is the hippocampus, which plays a central role in learning and memory.

Hippocampal atrophy is commonly observed in Alzheimer’s disease [7].

But here’s an important scientific distinction.

Not all brain shrinkage is Alzheimer’s disease, and reduced brain volume does not automatically mean someone will develop dementia.

The structural changes associated with severe nutritional deprivation are not necessarily caused by the same biological mechanisms responsible for Alzheimer’s disease.

Alzheimer’s involves characteristic processes, including abnormal amyloid-beta and tau accumulation, synaptic dysfunction, and progressive neurodegeneration.

Some brain-volume changes associated with severe undernutrition can improve with nutritional rehabilitation.

These are not identical processes.

Nevertheless, both observations demonstrate why maintaining brain health is important.

If a person is losing substantial weight, we should be concerned about preserving not only skeletal muscle but also the nutritional conditions necessary for normal neurological function.

Mitochondria, Nutrients, and the Brain’s Energy Supply

Another important piece of this physiological puzzle involves mitochondria.

Mitochondria are structures inside our cells responsible for producing much of the ATP required for normal cellular activity.

Neurons are especially dependent on mitochondrial energy production.

Your brain cells require ATP to transmit electrical signals, maintain cellular balance, transport materials, and communicate with neighboring neurons.

During a calorie deficit, the body can obtain energy from stored fuels.

But normal energy metabolism still requires essential nutrients.

For example, thiamine is necessary for enzymes involved in cellular energy metabolism.

Severe thiamine deficiency can cause serious neurological injury.

Vitamin B12 deficiency can interfere with neurological function and may contribute to cognitive symptoms.

Iron participates in oxygen transport and numerous metabolic processes.

Essential fatty acids help maintain the structure and function of neuronal membranes.

The brain needs more than calories. It needs the nutrients required to maintain healthy cells and use energy effectively.

That is why prolonged nutritional inadequacy deserves attention, regardless of whether it results from illness, restrictive dieting, or medication-associated appetite suppression.

Essential Fatty Acids and Brain Cell Membranes

One area of nutritional neuroscience that deserves attention involves the fatty acids that help make up neuronal cell membranes.

Docosahexaenoic acid (DHA), an omega-3 fatty acid, is particularly abundant in brain cell membranes.

DHA contributes to membrane organization and neuronal signaling.

Eicosapentaenoic acid (EPA), another omega-3 fatty acid, participates in biological pathways involved in inflammatory regulation.

Omega-6 fatty acids also perform essential physiological functions.

The body requires certain essential fatty acids from the diet because it cannot manufacture them from scratch.

When food intake becomes substantially restricted, the amount of these nutrients consumed may also decline.

However, the relationship between fatty-acid intake, blood biomarkers, brain health, and Alzheimer’s disease is complex.

We do not currently have evidence demonstrating that GLP-1 medications cause Alzheimer’s disease by changing omega-6 or omega-3 status.

Nevertheless, ensuring adequate essential fatty-acid intake remains an important part of comprehensive nutritional care.

Adults Age 65 and Older: Why I Am Particularly Concerned

Now let’s discuss a population that I believe deserves special attention.

Adults age 65 and older.

As more older adults use GLP-1 medications to manage obesity and type 2 diabetes, we need to consider how substantial appetite suppression interacts with the physiological changes associated with aging.

One of those changes is the progressive loss of skeletal muscle.

When muscle loss becomes clinically significant and is accompanied by reduced strength or physical performance, it may contribute to sarcopenia.

Sarcopenia is associated with weakness, falls, disability, and loss of independence.

Skeletal muscle also plays a major role in glucose disposal and insulin sensitivity.

Older adults may already have reduced muscle reserves before beginning a weight-loss medication.

If appetite suppression leads to inadequate protein intake, additional muscle loss may become a serious concern.

A 2026 review examining protein inadequacy during GLP-1 and GIP/GLP-1 treatment highlighted the possibility that absolute protein intake can decline even when protein continues to represent a similar percentage of total calories [8].

This is an important distinction.

A person may appear to be eating a reasonably balanced diet in percentage terms but still consume too little protein because their total food intake has fallen substantially.

Sarcopenic Obesity: When Excess Body Fat Hides Muscle Loss

Another important concern is sarcopenic obesity.

This occurs when someone has excess body fat alongside reduced muscle mass and function.

An older adult with sarcopenic obesity may appear overweight while already having limited muscle reserves.

Now imagine that person begins taking a medication that substantially suppresses appetite.

They may lose 30 or 40 pounds.

But if they aren’t consuming adequate protein or participating in appropriate resistance exercise, some of that weight loss may involve additional lean tissue.

It’s also important to distinguish lean mass from skeletal muscle.

Lean mass includes water, organs, muscle, and other nonfat tissues.

Therefore, a reduction in lean mass does not necessarily mean the same amount of skeletal muscle has been lost.

Still, muscle preservation is a legitimate concern during substantial weight loss, particularly in older adults [5, 8].

For older adults, successful weight loss should mean improved health and physical function—not simply a lower body weight.

The Aging Brain Has Less Room for Nutritional Mistakes

The aging brain undergoes physiological changes.

Some degree of brain-volume reduction occurs with normal aging.

Older adults may also experience changes in cerebral blood flow, vascular function, and metabolic regulation.

And advancing age is the strongest established risk factor for Alzheimer’s disease [7].

This means nutritional deficiencies may be particularly consequential in older adults who already have medical conditions or limited physiological reserves.

Consider a 72-year-old person who begins taking a GLP-1 medication.

Over several months, they lose 35 pounds.

Their physician is pleased.

Their family celebrates.

But what if this person is consuming insufficient protein?

What if they’re losing strength?

What if they’re developing a vitamin B12 or thiamine deficiency?

What if persistent nausea makes it difficult to consume adequate meals?

The weight loss might improve blood glucose, blood pressure, and other metabolic indicators.

But those improvements do not eliminate the possibility of nutritional complications.

We should not celebrate a smaller body while overlooking declining strength, inadequate nutrition, or emerging neurological symptoms.

 

Could Nutritional Inadequacy Increase Dementia Risk in Older Adults?

This is the question I believe deserves greater scientific attention.

We know that advancing age increases dementia risk.

We know that severe nutritional deprivation can affect brain structure.

We know that certain nutritional deficiencies can cause neurological dysfunction.

And we know that substantial weight loss can involve reductions in lean tissue.

What we do not yet know is whether prolonged nutritional inadequacy during GLP-1 treatment increases future Alzheimer’s disease risk.

That causal relationship has not been established.

Furthermore, some research suggests that GLP-1 medications may be associated with favorable cognitive outcomes.

Nevertheless, nutritional complications and potential medication benefits are not mutually exclusive.

A medication could improve blood glucose regulation and cardiovascular health while an individual patient simultaneously experiences harm from inadequate nutrition.

That is why older adults deserve individualized assessment and monitoring.

The goal should be to improve metabolic health while preserving muscle, maintaining adequate nutrition, protecting cognitive function, and supporting independence.

What Recent Research Actually Says About GLP-1 Drugs and Dementia

The relationship between GLP-1 medications and dementia is more complicated than some headlines suggest.

A study published in Diabetes, Obesity and Metabolism examined dementia diagnoses among adults age 50 and older with type 2 diabetes who began different glucose-lowering medications [9].

Researchers compared GLP-1 receptor agonists with two other medication classes.

Compared with sodium-glucose cotransporter-2 (SGLT2) inhibitors, GLP-1 users had a 53% higher relative hazard of dementia diagnosis.

However, compared with dipeptidyl peptidase-4 (DPP-4) inhibitors, GLP-1 users had a 24% lower relative hazard of dementia diagnosis.

These were relative associations, not absolute probabilities.

The study was observational and did not establish that GLP-1 medications caused dementia.

It also did not demonstrate a statistically significant increase in Alzheimer’s disease specifically.

Nor did the researchers establish that calorie restriction, nutritional deficiencies, muscle loss, or changes in brain volume explained the results.

Other research has reported potentially favorable associations.

A 2025 systematic review and meta-analysis published in JAMA Neurology evaluated 26 randomized clinical trials involving 164,531 participants [10].

In the GLP-1 subgroup, treatment was associated with a statistically significant reduction in the combined outcome of dementia or cognitive impairment.

However, Alzheimer’s disease specifically was not significantly reduced.

The neurological event counts were relatively small, and follow-up was limited compared with the many years over which Alzheimer’s disease typically develops.

These findings are important.

The available evidence does not establish that GLP-1 medications cause Alzheimer’s disease.

In fact, some findings suggest potential neurological benefits.

But here’s the distinction I want readers to understand.

Potential neurological benefits of a medication do not eliminate the need to prevent malnutrition during treatment.

These are separate clinical questions, and both deserve attention.

The Physiological Domino Effect We Need to Investigate

Let’s connect the dots.

We know GLP-1 medications suppress appetite.

We know appetite suppression often reduces calorie consumption.

We know a calorie deficit is a major mechanism behind weight loss.

We know substantial reductions in food intake can make it more difficult to meet essential nutritional requirements.

We know severe nutritional deprivation can affect brain structure.

And we know certain patterns of brain atrophy are associated with cognitive decline and Alzheimer’s disease.

These observations establish a biological rationale for investigating the nutritional consequences of prolonged appetite suppression.

However, they do not establish that a calorie deficit causes Alzheimer’s disease.

Nor do they demonstrate that GLP-1 medications cause brain shrinkage through nutritional deprivation.

That specific causal pathway remains unproven.

Researchers need studies that evaluate dietary intake, nutritional biomarkers, body composition, muscle strength, brain imaging, cognitive performance, and long-term neurological outcomes.

These studies should also distinguish the effects of the medications from those of obesity, diabetes, vascular disease, aging, and weight loss itself.

We do not need to prove that GLP-1 medications cause Alzheimer’s disease to recognize that severe malnutrition can be harmful and should be prevented.

That is the central message I want people to understand.

What Responsible GLP-1 Treatment Should Include

I believe a responsible weight-management program should evaluate much more than pounds lost.

Healthcare professionals should consider the following throughout treatment.

Nutritional assessment: Evaluate food intake, dietary quality, and whether essential nutritional requirements are being met.

Protein adequacy: Establish individualized protein targets that support muscle preservation, particularly in older adults. Protein needs should account for kidney function, medical conditions, and other individual factors.

Resistance exercise: Encourage appropriate strength training to help preserve muscle and physical function.

Body composition and physical performance: When clinically appropriate, evaluate muscle strength, mobility, and body composition rather than relying exclusively on body weight.

Micronutrient status: Investigate possible deficiencies when dietary intake, symptoms, medical history, or other risk factors justify testing.

Essential fatty acids and dietary fiber: Encourage a nutritionally complete eating pattern that provides essential fats, adequate fiber, and appropriate dietary variety.

Hydration and gastrointestinal tolerance: Monitor persistent nausea, vomiting, dehydration, and difficulty maintaining adequate food intake.

Cognitive health: Evaluate new or worsening memory problems, confusion, or changes in everyday functioning.

Not every patient needs every laboratory test or intensive monitoring.

But older adults, people with sarcopenic obesity, frailty, persistent gastrointestinal symptoms, or pre-existing nutritional deficiencies may require additional attention [4, 5].

And no one should discontinue a prescribed GLP-1 medication without discussing the decision with their healthcare professional.

My Final Thoughts: Healthy Weight Loss Must Protect More Than the Waistline

For more than three decades, I’ve encouraged people to understand that losing weight and improving health are not necessarily the same thing.

And the growing popularity of GLP-1 medications makes that distinction more important than ever.

A person can lose substantial weight and improve blood glucose control.

But if they’re also losing excessive skeletal muscle, consuming insufficient essential nutrients, or developing preventable deficiencies, we need to ask whether their care is truly comprehensive.

The brain is one of the most metabolically demanding organs in the human body.

It requires a continuous supply of metabolic energy and essential nutrients.

Scientific research has demonstrated that severe nutritional deprivation can affect brain structure.

And certain patterns of brain atrophy are associated with cognitive decline and Alzheimer’s disease.

What remains unproven is whether nutritional inadequacy during prolonged GLP-1 treatment contributes to brain atrophy or increases Alzheimer’s disease risk.

That question deserves further investigation, especially among adults age 65 and older.

But we don’t need to wait for those studies to recognize the importance of preventing malnutrition.

I believe it is irresponsible to celebrate dramatic weight loss without also evaluating whether patients are receiving adequate nutrition, preserving skeletal muscle, and maintaining long-term physical and neurological health.

The responsibility of healthcare professionals should extend beyond writing prescriptions and monitoring the scale.

Patients deserve appropriate nutritional guidance, individualized care, and ongoing evaluation of their overall health.

Because the ultimate goal should never be to become thinner at any cost.

The goal should be to lose excess body fat while protecting the brain, preserving skeletal muscle, maintaining nutritional adequacy, and improving quality of life.

Scientific References

1. 1. Raichle, M. E., & Gusnard, D. A. (2002). Appraising the brain’s energy budget. Proceedings of the National Academy of Sciences, 99(16), 10237–10239. https://doi.org/10.1073/pnas.172399499
   2. Owen, O. E., Morgan, A. P., Kemp, H. G., Sullivan, J. M., Herrera, M. G., & Cahill, G. F., Jr. (1967). Brain metabolism during fasting. The Journal of Clinical Investigation, 46(10), 1589–1595. https://doi.org/10.1172/JCI105650
   3. Avoiding malnutrition in the era of glucagon-like peptide-1 medications: Emerging evidence and opportunities for integrated nutrition care. (2026). The Journal of Nutrition. https://jn.nutrition.org/article/S0022-3166(26)00333-0/fulltext
   4. Hidden malnutrition in the GLP-1 era: Micronutrient status, protein adequacy, and lean mass as emerging nutritional considerations—A narrative review. (2026). PubMed. https://pubmed.ncbi.nlm.nih.gov/42738931/
   5. Nutritional priorities to support GLP-1 therapy for obesity: A joint advisory from the American College of Lifestyle Medicine, the American Society for Nutrition, the Obesity Medicine Association, and The Obesity Society. (2026). https://pmc.ncbi.nlm.nih.gov/articles/PMC13237850/
   6. Structural brain alterations in anorexia nervosa: A global brain volume and anatomical likelihood estimation (ALE) meta-analysis combined with a functional decoding approach. (2026). NeuroImage: Clinical. https://www.sciencedirect.com/science/article/pii/S2213158226000094
   7. National Institute on Aging. (n.d.). What happens to the brain in Alzheimer’s disease? National Institutes of Health. https://www.nia.nih.gov/health/alzheimers-and-dementia/what-happens-brain-alzheimers-disease
   8. Risk of protein intake deficiency during treatment with GLP-1 and GIP/GLP-1 receptor agonists: Considerations for secondary sarcopenia. (2026). PubMed. https://pubmed.ncbi.nlm.nih.gov/42631799/
   9. Zhou et al. (2026). Association between glucagon-like peptide-1 receptor agonists and risk of dementia in older adults with type 2 diabetes: A target trial emulation. Diabetes, Obesity and Metabolism. https://doi.org/10.1111/dom.70384
   10. Seminer, A., Mulihano, A., O’Brien, C., et al. (2025). Cardioprotective glucose-lowering agents and dementia risk: A systematic review and meta-analysis. JAMA Neurology, 82(5), 450–460. https://doi.org/10.1001/jamaneurol.2025.0360

__________
Robert Ferguson is a California- and Florida-based single father of two daughters, clinical nutritionist, Omega Balancing Coach™, researcher, best-selling author, speaker, podcast and television host, health advisor, NAACP Image Award Nominee, creator of the Diet Free Life methodology, and Chief Nutrition Officer for iCoura Health. He also serves on the Presidential Task Force on Obesity for the National Medical Association and the Health and Product Advisory Board for Zinzino, Inc.

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