Most people are aware of type 1 and type 2 diabetes, but did you know there is a type 3 diabetes as well! It is a more obscure term. Although it is not an accepted medical diagnosis, type 3 diabetes has been discussed in the literature as a possible relationship between insulin resistance in the brain and Alzheimer's disease. This link has been described to help explain how metabolic disorders impact brain health, causing cognitive decline and dementia.

What is Type 3 Diabetes?

Type 3 diabetes is more of a misnomer because it should not be confused with type 3c diabetes, which relates to pancreatic dysfunction. The term "type 3 diabetes," on the other hand, has been loosely used by some scientists to analogously propose that Alzheimer's disease is strongly implicated with insulin resistance in the brain.

This concept was conceptualized by Dr. Suzanne de la Monte and Dr. Jack Wands of Brown University in the year 2008. This hypothesis postulated that Alzheimer's disease may be called type 3 diabetes for it bears many similarities with glucose metabolism disorder type 2 diabetes. Their concept arises from the basic principle that insulin is fundamental to blood sugar regulation, but it is also the case with the brain. When brain cells become insulin-resistant, they lose access to glucose, impairing their function.

Research published in the Journal of Diabetes Science and Technology supports this hypothesis by indicating that insulin resistance can be a significant contributor to the occurrence of dementia, also referred to as Alzheimer's. The symptoms of memory loss and diminished reasoning are associated with impaired glucose metabolism in the body, especially in the cerebral tissue.

Symptoms of Type 3 Diabetes

Although type 3 diabetes is not a "medical term," its symptoms correlate well with Alzheimer's diseases that are known to reduce the ability to think in an efficient manner and bring down brain health. These signs are:

- Loss of memory, especially short-term.

- Poor judgment and judgment ability

- Failure in recognizing people or places familiar once.

- Failure in the process of reading, writing or processing numbers

- Anxiety, agitation, or mood changes.

- Disorganized thoughts or confusion

- Lack of impulse control

As the disease advances, patients may be afflicted with severe complications including an inability to swallow or control their bodily functions. In the final stages, most patients die from fatal complications such as aspiration pneumonia.

Causes of Type 3 Diabetes

This may not be well understood with regards to type 3 diabetes, or the exact link between insulin resistance and Alzheimer's disease. Some identified contributing factors include the following:

1. Insulin Resistance

Insulin acts as an important regulatory mechanism of brain functions such as memory and cognition. The reduction in insulin signaling may impair metabolism of brain cells, thus bringing about neurodegeneration.

2. Type 2 Diabetes

These diseases show a strong relationship and those individuals diagnosed with type 2 diabetes have double chances of getting Alzheimer's. In the two, the main causes can be chronic inflammation, oxidative stress, and a defect in glucose metabolism.

3. Environmental and Lifestyle Factors

Insulin resistance associated with obesity, stress, and an unhealthy diet is considered a cause that may increase the chances of Alzheimer's disease.

Researches in Frontiers in Neuroscience and The Lancet Neurology have also highlighted that drugs used for antidiabetic medication may be crucial for the prevention or at least slowing down the course of Alzheimer's.

Treatments for Type 3 Diabetes

In 2022, in a study in Pharmaceuticals, researchers studied biomarker uptake in brain regions implicated in the faulty uptake and metabolism of blood sugar in Alzheimer’s patients.

Emerging Therapies

Research into such treatments as intranasal insulin has also been promising. Intranasal delivery of insulin directly to the brain has been reported to enhance glucose uptake by brain cells, improve memory, and boost cognitive performance. While such clinical trials have been shown to be successful, additional research is needed for safety and efficacy.

Medications

For patients being aggressive or agitated, antipsychotic drugs may be prescribed; however, therapies such as cognitive rehabilitation as well as cognitive stimulation therapy serve to preserve memory and executive function.

Lifestyle Interventions

Diet, exercise, and stress management are critical in preventing and managing insulin resistance. A review in the Journal of Alzheimer's Disease also highlighted the benefits of Kirtan Kriya meditation, which can regulate genes involved in insulin and glucose metabolism, improve sleep, and reduce inflammation.

Can Type 3 Diabetes Be Prevented?

Although type 3 diabetes is not officially recognized, its connection to Alzheimer’s disease underscores the importance of proactive measures for brain health. Some prevention strategies include:

1. Healthy Diet

Consuming a balanced diet rich in antioxidants, whole grains, and healthy fats may support brain health.

2. Regular Exercise

Physical activity improves insulin sensitivity, reduces inflammation, and enhances overall metabolic health.

3. Stress Reduction

Mindfulness practices, including meditation, have been shown to lower stress levels, which can reduce the risk of cognitive decline.

The term type 3 diabetes brings out the complex relationship between metabolic disorders and brain health. Even though it is not a recognized medical condition, the concept emphasizes the crucial role of insulin in brain function and its possible contribution to Alzheimer's disease. Continued research will hopefully provide hope for therapies such as intranasal insulin and lifestyle modifications.

People living with obesity and diabetes often feel healthy in their day-to-day life, but some of the most dangerous changes may be happening silently inside their bodies.

The liver is one of the first organs to be affected. In many cases, fat slowly accumulates in the liver without causing any pain, discomfort, or obvious symptoms. This is why fatty liver disease is often called a “silent condition.” By the time it is detected, it may already have progressed to an irreversible stage.

Excess body fat, particularly around the abdomen, disrupts how the body processes sugar and fats, placing continuous stress on the liver. Because of this silent progression, experts now strongly recommend that people living with obesity and type 2 diabetes should proactively check their liver health, even when they feel completely well.

Obesity is closely linked with liver damage through a series of metabolic changes that develop over time. When the body becomes resistant to insulin, fat begins to accumulate in liver cells, triggering inflammation and gradual injury.

If this continues unchecked, the condition can progress from simple fat accumulation to more serious stages, including metabolic dysfunction-associated steatohepatitis (MASH), where inflammation and liver cell damage become more significant.

Over time, this may lead to fibrosis (scarring of the liver), and in advanced cases, cirrhosis, which can severely affect liver function. Further, patients with fatty liver may directly present with liver cancer, which can occur in up to 20% of patients.

How Common Is Fatty Liver In People With Diabetes And Obesity?

In India, the burden of metabolic dysfunction-associated steatotic liver disease (MASLD) or fatty liver is rising and is now recognised as a common metabolic condition. Studies from the Indian subcontinent estimate that 1 in 3 people may have MASLD. Fatty liver is particularly common among individuals with metabolic risk factors.

It is seen in nearly 40–80% of people with type 2 diabetes and 30–90% of those with obesity, often without clear symptoms.iv Hospital-based trends also suggest increasing detection in younger age groups, reflecting changes in diet, reduced physical activity, and more sedentary lifestyles.

Also read: Post-Menopausal Women Face A Higher Risk Of Fatty Liver Disease: How Falling Estrogen Levels Impact Liver Health

What Liver Checks And Preventive Measures Should You Follow?

Preventive measures to be followed:

• If you live with excess weight/obesity and type 2 diabetes or PCOS (polycystic ovarian syndrome) or dyslipidemia, seek early consultation with a physician or hepatologist.

• Your doctor may request routine metabolic screening:

• Regular liver function tests as part of annual health check-ups

• Ultrasound screening for individuals with obesity or diabetes

• Monitoring blood sugar, cholesterol, and triglyceride levels

• Liver scarring scan (annually for patients with diabetes/obesity)

• Avoiding long-term neglect of “mild” or borderline test results

Also read: From Liver Inflammation to Cancer: When Hepatitis Becomes a Serious Warning Sign

With rising obesity rates in India, early liver screening should become a routine part of preventive healthcare. Even modest weight reduction, improved diet quality, and regular exercise (approximately 150 minutes per week of moderate-intensity exercise (example: brisk walking, gardening, swimming, cycling) or 75 minutes of vigorous exercise (example: weight training) can significantly reduce liver fat and inflammation within 3-6 months.

However, once the disease progresses to MASH or fibrosis, reversal becomes more difficult and may require long-term medical management. Early-stage fatty liver disease is reversible in many cases. In fact, medications can even reverse liver fibrosis (early scarring), but in only 25% of patients. Simple homemade food is sufficient to prevent these lifestyle diseases, and there is no need for “fancy online diets or supplements”.

Our forefathers lived longer by consuming homemade food and water without any supplements. Newly approved therapies such as semaglutide (GLP1 analogues) have been shown to resolve steatohepatitis and reduce liver fibrosis. These liver benefits do not appear to be explained solely by weight loss, suggesting a broader potential impact on liver health.

The absence of symptoms does not mean the absence of risk. Taking care of the liver early is not just about preventing disease; it is about protecting long-term health, energy, and quality of life.

By Dr. Anand V. Kulkarni, Senior Consultant Hepatologist & Director – Critical Care Hepatology, AIG Hospitals, Hyderabad

There is a conversation that comes up in almost every consultation, and it is rarely the one the patient came prepared for. After graft numbers, hairline design, cost and downtime have been discussed, the question of smoking and drinking inevitably follows — and the answer is usually a shrug: occasionally, socially, nothing serious.

Yet of all the variable that determines what a patient sees in the mirror eighteen months later, these two are among the very few fully within their control, and among the most underestimated.

What Smoking and Alcohol Do to the Scalp

The hair follicle is one of the most metabolically demanding structures in the body, dividing faster than almost any other cell population and depending entirely on a dense network of microscopic vessels feeding its base. Nicotine constricts those vessels; over years, repeated narrowing combined with low-grade inflammation contributes to perifollicular fibrosis — scarring that gradually chokes the follicle.

Alcohol takes a different route, depleting the zinc, iron, folate, B12 and protein hair is built from, while fragmenting sleep and raising cortisol — both of which push follicles prematurely into their resting phase. For a transplant candidate, this matters twice over: it reflects donor-area quality, and it signals the kind of healing environment the grafts are about to enter.

Also read: The Hidden Health Risk of Sitting for Long Hours: What Young Professionals Need to Know

Why the First Week After Surgery Is So Critical

For the first few days after surgery, a transplanted follicle is essentially cut off from its blood supply, surviving on nutrients diffusing in from surrounding tissue.

New capillaries begin connecting around day four or five, with full revascularisation taking seven to ten days — the most vulnerable window in the graft's life. Smoking attacks it from two directions: nicotine causes sustained vasoconstriction after every cigarette, while carbon monoxide binds haemoglobin more readily than oxygen, so the reduced blood reaching the scalp also carries less oxygen.

The result is rarely dramatic — just poorer graft survival, patchier density, and a final outcome thinner than the graft count promised. Patients often read this as bad luck; it usually isn't. Notably, this applies equally to vaping, hookah and smokeless tobacco like gutkha or khaini — the delivery method changes, but the nicotine doesn't.

Also read: Ozempic/Wegovy Vs Zepbound/Mounjaro: Which Weight Loss Drug Is More Likely To Cause Hair Loss? Study Finds

Alcohol's More Immediate Risk

Alcohol's damage is more mechanical. It causes vasodilation and impairs clotting, meaning patients who've been drinking beforehand bleed more during surgery — which makes graft placement less precise and can dislodge grafts already sited.

Afterward, the same vasodilation worsens normal post-op swelling, its diuretic effect fights the hydration healing tissue needs, and its immune-suppressing effect arrives just as the scalp carries thousands of small open wounds. There's a medication risk too: alcohol combined with post-op antibiotics, anti-inflammatories or steroids raises the chance of gastric irritation or a genuinely unpleasant systemic reaction.

Recommended Windows

For smoking: stop at least two weeks before surgery (four is better), and stay off it for two weeks to a month afterwards — the long lead-in accounts for how slowly small-vessel and immune function normalise, and the long tail covers graft revascularisation.

For alcohol: stop five to seven days before, and avoid it for ten to fourteen days after, or as long as medication continues, since its effects reverse faster. One caveat worth repeating: patients often say they've "stopped" when they've merely cut back. A single cigarette produces measurable scalp vasoconstriction — in this window, occasional isn't the same as fine.

Also read: Love Travelling? Here's How Flying Frequently Impacts Your Health

The Myth That Lifestyle Stops Mattering

A costly misconception is that once surgery is done, lifestyle no longer matters. It's a half-truth: transplanted follicles, taken from the DHT-resistant back and sides of the scalp, are permanent and won't miniaturise. But a transplant only redistributes existing hair — every native follicle remains susceptible to ongoing loss.

If that native hair keeps thinning, overall density falls even though every graft survives, and patients often mistake this for transplant failure. In reality, the surroundings have receded, accelerated by smoking, poor sleep, chronic stress and poor nutrition. Surgery buys a foundation; lifestyle determines how long the picture around it holds.

Practical Guidance

Honesty at consultation matters — knowing a patient smokes heavily changes the surgical plan toward more conservative density and staging, which protects the result. The pre- and post-op window should be treated as non-negotiable, even if permanent quitting feels distant; a defined four-week commitment is far more achievable than an open-ended one.

Switching to vaping or nicotine gum isn't automatically safe — it removes carbon monoxide and tar, but nicotine, the actual vasoconstrictor, remains, so replacement therapy should be discussed with the surgeon. Fundamentals also help: adequate protein, iron and vitamin D, seven to eight hours of sleep, hydration, and gentle movement once cleared.

Turning Surgery into Leverage

Finally, surgery itself can be motivating. Patients who've just invested significant money and recovery time in their appearance are often more driven to quit than at any other point in

By Dr. Harikiran Chekuri, Hair Transplant Surgeon, Founder and Chief Plastic Surgeon, Redefine Hair Transplant & Plastic Surgery Center

It is difficult to determine emotions because of the neurological differences, the surrounding in childhood, the psychological ways of survival, and absence of emotional training.

Alexithymia or "emotional blindness" is the neuropsychological trait associated with severe problems with identification, recognition, and description of the person's emotions. Alexithymia is not a psychiatric disease but a personality trait.

It is characterized by the inability to identify and distinguish emotions and body sensations, difficulty of finding the words to express feelings, inability to understand facial expression and body language of another person and emotional detachment during stressful situations.

It is diagnosed in people with autism spectrum disorder, depressive disorder, generalized anxiety disorder and after traumatic brain injuries. It can be inherited or acquired as a result of childhood trauma, abuse or neurological damage.

The Brain Science Behind Alexithymia

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The cause of alexithymia is the brain wiring and neurological differences. Therefore, there is impaired interception, which is the inability of the brain to recognize its own physical sensations. Also, an unusual structure of the brain regions like amygdala and insula, that regulate emotions, makes difficult to decode emotional signals.

Early childhood environment and emotional competence must be developed in childhood, because, without that, there can be emotional neglect and emotional vocabulary deficiency. Due to the inability to interpret emotional data, the person misses the compass that directs decisions and self-calming. This leads to emotional outburst, panic, hyperarousal, social and psychological consequences.

How Alexithymia Differs From Emotional Numbness

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Emotional numbness is the transient psychological state caused by acute trauma, deep grief or burnout.

The lack of emotional intelligence is the lack of social and emotional competence, when the person feels his emotions correctly, but he cannot control temper, lacks empathy, makes inappropriate social decisions or do not know what kind of effect his behaviour causes on the room.

But alexithymia is different since it is long-term personality trait and the person is unaware of the particular emotion.

In terms of neurodevelopment, the insular cortex and the anterior cingulate cortex (ACC) are the structural core of the brain's salience network. They work as a translator, transforming chaotic physical sensations into recognizable emotional experience.

Although there isn't any cure for alexithymia, one can improve his emotional awareness through certain measures. Interoceptive training where individuals are taught how to associate physical body sensations (such as tightness in the chest) with particular emotions (such as stress).

The use of emotion wheel or list of emotional words to bridge the link between vague physical sensation and precise description. Mindfulness, which involves observing oneself without judgment or without trying to suppress those internal feelings right away. And it is always good to seek professional help from a psychologist or a counselor.

By Dr. Arun Shah, Director - Neurosciences, Sir H.N. Reliance Foundation Hospital