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.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously called fatty liver disease, is becoming extremely common in people with type 2 diabetes in India.

Studies suggest that 50–70 percent of Indians with type 2 diabetes may have fatty liver, and a significant proportion can progress to inflammation, liver fibrosis, cirrhosis, or even liver cancer if the condition is not detected early. Because India already has one of the world’s largest populations with diabetes, MASLD is emerging as a major but under-recognized public health problem.

The recently published consensus guidelines developed by Indian experts aim to provide practical, India-specific recommendations for diagnosing and managing MASLD in people with type 2 diabetes.

In fact, these are the first global guidelines for MASLD and type 2 diabetes, albeit restricted to India. This matters because most existing international guidance—including from organizations such as the American Diabetes Association—is largely based on evidence and healthcare systems in high-income Western countries. These recommendations often assume easy access to expensive diagnostic tests and medications, which may not always be feasible in India.

In India, healthcare costs are frequently paid out-of-pocket by patients. Advanced imaging tests or newer medications can therefore be unaffordable for many people.

The Indian consensus addresses this reality by recommending step-wise and cost-effective screening strategies, beginning with simple clinical risk assessment and basic laboratory tests, followed by non-invasive fibrosis scoring tools and ultrasound when appropriate. This approach helps identify high-risk individuals without overburdening patients or the healthcare system.

Another important reason these guidelines matter is that Asian Indians have a unique metabolic profile. Compared with Western populations, Indians often develop diabetes and fatty liver at younger ages and lower body weight, partly because of higher abdominal fat and insulin resistance. Therefore, early screening for liver disease in people with diabetes becomes particularly important in India.

Dietary recommendations are also adapted to local eating patterns. Instead of focusing on Western dietary models, the guidelines emphasize reducing refined carbohydrates, excess sugars, and unhealthy fats common in Indian diets while promoting traditional, healthier foods, whole grains, legumes, and increased physical activity.

In simple terms, these India-specific guidelines aim to ensure that more patients with diabetes are screened early, treated appropriately, and protected from severe liver complications, using strategies that are practical, affordable, and suited to the realities of the Indian healthcare system.

How These Guidelines Differ From Those In The West

Guidelines for MASLD developed in Western countries provide important scientific guidance, but they are often designed for healthcare systems with greater resources and different patient characteristics. The Indian consensus recommendations differ in several key ways to make them more suitable for local populations and healthcare settings.

First, screening strategies are more pragmatic and cost-conscious. Western guidelines often recommend advanced imaging tests or specialized biomarkers to assess liver fat and fibrosis. However, these tests can be expensive and not widely available in many parts of India.

The Indian recommendations emphasize simple, widely available tools—such as routine blood tests and non-invasive fibrosis scoring systems—before considering more advanced imaging. This stepwise approach ensures that patients who are most at risk are identified while keeping costs manageable.

Second, the guidelines recognize the unique metabolic risk profile of Asian Indians. Compared with Western populations, Indians tend to develop metabolic diseases such as type 2 diabetes and fatty liver at younger ages and lower body mass index (BMI). Abdominal obesity and insulin resistance are particularly common.

Therefore, the Indian recommendations stress earlier and more vigilant screening for MASLD in people with diabetes, even if they are not severely obese.

Third, treatment priorities differ because of affordability and access to medications. Western guidelines may emphasize newer and often expensive drugs that show benefits for fatty liver disease. While these therapies can be effective, they may not be accessible to many patients in low- and middle-income countries.

The Indian consensus places stronger emphasis on lifestyle interventions, weight reduction, improved diet, and physical activity as the foundation of treatment, while suggesting pharmacotherapy selectively based on evidence, availability, and cost.

Fourth, perhaps the most important difference, dietary advice is culturally tailored. Western guidelines typically discuss Mediterranean-style diets.

In contrast, the Indian recommendations translate healthy eating principles into Indian dietary patterns, focusing on reducing refined carbohydrates, sugar-sweetened foods, and excess saturated fats while promoting whole grains, pulses, vegetables, and traditional balanced meals.

Finally, the Indian document highlights the need for public health awareness and primary care involvement, since a large proportion of patients with diabetes are managed outside specialized centers.

Overall, the key difference is that while Western guidelines provide strong scientific foundations, the Indian recommendations adapt those principles to local realities.

Bristol Palin, an American real estate agent, who was a former public speaker and reality television personality started experiencing facial paralysis over a tear ago. On March 9, her 35-year-old daughter Sarah Palin posted a video on her Instagram Stories that shared an update on her ongoing health struggles. The story revealed that she is now considering plastic surgery to fix her paralysis.

"I am going to have a consultation today with a plastic surgeon in Austin," she said. "I have read that she specializes in facial paralysis type stuff so we will see what she says."

She also said, "Prayers because maybe she can help mostly with this eye," while pointing to her left eye. "When I smile or when I am expressive, it closes. I don't really care about my crooked mouth but my eye...so embarrassing to me. I feel like I should wear an eyepatch or something."

She went on to say, "It looks crazy and I just feel like I cannot even smile because it just closes. So maybe she can do some Botox or maybe there is some options with surgery. So we will see. Maybe she ca help with this eye or just the overall symmetry."

She also said that she had just returned from Alaska, where she visited another specialist who does her facial nerve blocks to help her paralysis. She also posted another update on her Instagram Stories and said that her consultation went well and that she will be sharing the information with her followers soon.

What Happened To Bristol Palin?

It was in January 2025, when she revealed her facial paralysis on Instagram. "I woke up nine days ago with a little weird sensation in my face. My mouth was pulling this way and it just felt a little off. So I went, looked in the mirror. I'm like 'Wow. This is looking a little weird. I feel like everything is pulling to the left."

She said that hours later her condition got worse and the left side of her face was having a "delayed" reaction.

Read: Why Does Your BBL Smell? Doctor Explains 4 Reasons That Could Cause It

Can Botox Fix Asymmetrical Face?

As per a 2020 study published in the Indian Journal of Plastic Surgery, botulinum toxin (Botox) injections are helpful and are minimally invasive technique to restore facial symmetry. However, the study noted that a "surprisingly small minority of aesthetic injectors treat this condition."

The study also gives a case study of a patient with longstanding facial nerve paralysis after resection of an osteogenic sarcoma, before and after two weeks after first treatment with botulinum toxin. The improvements could be seen in mentalis synkinesis, more symmetrical smile, and improved eye apertures on animation.

What Is Botox?

It is an FDA-approved, injectable neurotoxin derived from Clostridium botulinum bacteria. It temporarily relaxes muscles by blocking nerve signals, commonly used to smooth dynamic wrinkles and treat medical conditions like chronic migraines, excessive sweating, and muscle spasms. Its effects last from three to four months.

Botox prevents the release of a neurotransmitter that signals muscles to contract, causing them to relax and soften wrinkles. Results typically appear in 3 to 14 days.

The US Food and Drug Administration approved leucovorin for cerebral folate deficiency in the receptor 1 gene, a rare genetic condition. However, last year, in September, this drug was noted as the possible and potential treatment for children with autism. The Trump administration noted that Tylenol may be triggering autism in children when is consumed by pregnant mothers. The same conference touted this drug as a potential treatment, while not enough scientific evidence was there to support the claim. Yet, many parents looked for the prescription to support their children.

Health and Me also reported a story of a mother who looked for the drug for her three-year-old son. Another case of four-year-old Jose Morales-Ortiz, who struggled to speak even two-word sentences. As per a CNN report, he was diagnosed with severe autism and rarely responded when someone called his name.

However, something changed, in early summers, he began telling his guardian Keith Joyce about the conversation with his classmates and answering follow-up questions. For Keith, it was a moment of joy. It was also the first time Keith had a conversation with him.

Joyce believes the change began after Jose started taking leucovorin, a medication originally approved to reduce the side effects of certain chemotherapy drugs. Now, researchers are investigating whether the drug may help some children with autism—particularly those with a condition known as cerebral folate deficiency.

However, scientists caution that while early studies are promising, the evidence is still limited and the treatment remains controversial.

What Is Leucovorin?

Leucovorin, also known as folinic acid, is a biologically active form of vitamin B9 or folate. Unlike standard folic acid supplements, it does not require the body to convert it into an active form before it can be used. Due to this very feature, it can bypass certain metabolic steps and deliver folate more directly to the cells.

It is a high-dose B vitamin, which is commonly used as a treatment to counteract the side effects of chemotherapy. It has been approved by the FDA for cerebral folate deficiency in the receptor 1 gene. The disease is rare and fewer than 50 cases have been identified worldwide. FDA Commissioner Dr Marty Makary called this approval "a significant milestone" for patients with the condition.

Doctors have used the drug for several purposes, which also include:

• Reducing toxic side effects of chemotherapy
• Enhancing the effectiveness of certain cancer treatments
• Treating folate deficiency caused by medications or disease

Recently, scientists began exploring whether leucovorin could also help certain neurological conditions.

Read: Leucovorin Approved By FDA But For A Rare Genetic Disease, Not For Autism

What Role Does Folate Play In Brain Development?

Folate is essential for brain development and neural function.

It helps in:

• DNA synthesis and repair
• Formation of neurotransmitters
• Development of neural connections
• Cell growth in the developing brain

During pregnancy, folate is so critical that many countries fortify foods with folic acid to prevent birth defects such as neural tube defects.

However, in some children, the issue may not be a lack of folate in the diet—but a problem with how folate reaches the brain.

What Happens In Cerebral Folate Deficiency?

In 2005, researchers discovered an unusual phenomenon in some children with developmental disorders.

Although their blood folate levels were normal, their brain folate levels were extremely low.

The reason appeared to be autoantibodies—immune proteins that mistakenly attack the body’s own tissues. In this case, the antibodies targeted folate receptor alpha, the protein responsible for transporting folate across the blood-brain barrier.

When these receptors are blocked:

• Folate cannot enter the brain efficiently
• Neural development may be affected
• Symptoms similar to autism may appear

This condition is called cerebral folate deficiency.

Researchers also developed a diagnostic blood test called the Folate Receptor Autoantibody Test (FRAT) to detect these antibodies.

How Does Leucovorin Work?

It could work in such a case because it is able to bypass the blocked folate receptors. It does not rely on the usual transport system and is able to enter the brain through alternative transport pathways, which allow neurons to access the folate they need. Scientists also believe that this could improve neurotransmitter production, support neural communication, and enhance brain metabolism in certain children.

Some clinical studies have suggested that leucovorin may improve language and communication skills in certain children with autism.

In small trials:

• Some children showed improvements in expressive speech
• Others improved in receptive language and social communication
• Benefits appeared strongest in children with folate receptor antibodies

However, the results have been mixed.

Some studies have found only modest improvements, and large placebo-controlled trials—considered the gold standard in medical research—are still lacking.

Because autism is a complex spectrum condition with many biological pathways involved, researchers emphasize that no single medication is likely to work for every child.

The growing interest in leucovorin reflects a broader shift in autism research: looking for biological subtypes of the condition that might respond to targeted treatments.

If cerebral folate deficiency proves to be one of those subtypes, leucovorin could become an important therapy for a specific group of children.

But scientists emphasize that autism is highly complex. “There’s no autism pill,” many researchers say.