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If a cell doesn't receive enough insulin, it leads to impaired glucose uptake and utilisation, resulting in hyperglycaemia (high blood sugar levels). Here's what happens:

Insulin facilitates the entry of glucose into cells by promoting the translocation of glucose transporter proteins (GLUT4) to the cell membrane. Without sufficient insulin, GLUT4 remains sequestered inside the cell, preventing efficient glucose uptake.

Cells, particularly muscle and adipose tissue, become "starved" of glucose, their primary energy source, despite high blood glucose levels. This is known as insulin resistance.

The pancreatic beta cells attempt to compensate by increasing insulin secretion to overcome the resistance. However, if insulin production becomes inadequate due to beta cell dysfunction or destruction, hyperglycaemia persists.

Persistent hyperglycaemia leads to glucotoxicity, which further impairs beta cell function and insulin secretion, creating a vicious cycle.

Without sufficient insulin action, cells cannot effectively utilise glucose for energy production or storage. This leads to increased glucose production by the liver (gluconeogenesis) and impaired glucose uptake by peripheral tissues, exacerbating hyperglycaemia.

Chronic hyperglycaemia can lead to the development of type 2 diabetes mellitus if the insulin resistance and beta cell dysfunction are not addressed.

In summary, when cells don't receive enough insulin, they become insulin resistant, unable to take up and utilise glucose effectively. This leads to persistent hyperglycaemia, which can further impair beta cell function and insulin secretion, ultimately contributing to the development of type 2 diabetes if left unchecked

Yes, human cells tend to process insulin less efficiently as we age. Here are the key points to remember:

As we get older, our cells become more resistant to insulin (insulin resistance), making it harder for insulin to facilitate the absorption of glucose from the bloodstream into cells. This leads to higher blood sugar levels.

The exact mechanisms behind age-related insulin resistance are complex, but factors like changes in body fat distribution, increased inflammation, and altered mitochondrial function play a role.

Studies show that insulin sensitivity decreases with age, meaning cells become less responsive to insulin's effects. This reduced insulin sensitivity contributes to higher blood sugar levels in older adults.

While pancreatic beta-cell function (insulin production) may not necessarily decline with age alone, the combination of increased insulin resistance and potentially reduced insulin production can impair glucose homeostasis as we get older.

The age-related increase in insulin resistance and decrease in insulin sensitivity is thought to be a key factor linking aging to the higher risk of developing type 2 diabetes later in life.

In summary, multiple studies cited in the search results confirm that cellular processing and responsiveness to insulin becomes less efficient with increasing age, which can dysregulate blood sugar control and increase the risk of type 2 diabetes in older adults.

Physiologic Insulin Resensitization (PIR) is a revolutionary, multi-patented approach that treats the primary cause of diabetes – metabolic failure – by using insulin as a hormone instead of a drug, in other words using insulin in the same way that your pancreas does.

By replicating natural physiology with insulin, we are better able to combat insulin resistance and facilitate glucose entry into cells, which can then be converted into energy. The results are exciting and are giving many diabetics their life back.

By boosting cellular energy, tissue and organs that have been compromised can grow, heal, and regenerate. Research has demonstrated that this treatment method can be effective in stabilising, and in some cases even reversing, the effects of diabetes and other metabolic issues.

PIR is a patient-specific, clinic-based, tailored therapeutic approach that aims to mimic the body's natural pulsatile pattern of insulin secretion to improve insulin sensitivity and overcome insulin resistance.

With PIR, insulin is administered as a hormone rather than a drug; addressing the primary cause of diabetes which is metabolic failure. By utilising insulin in a manner that bio-mimics your normal physiology, this modality is designed to help physicians reduce insulin resistance which helps blood sugar more readily enter each cell and be converted into energy.

Increasing cellular energy allows damaged tissues and organs to grow, repair, and regenerate. Thus, our approach not only stabilises but in many instances has actually reversed complications of diabetes and other metabolic disorders.

PIR includes an intravenous precision administration of fast-acting insulin using a programmable portable pump.

The objective of the physician’s precisely tailored dosing is to achieve biomimicry of insulin as a hormone communicator to stimulate the metabolism–not to simply use insulin as a drug to suppress high blood sugar, which typically can eventually cause insulin resistance at the insulin receptor level.

The pump’s patented biomimicry engineering combined with the physician’s dosage protocol are designed to administer insulin bioidentically to the body’s way of maintaining an optimised metabolism.

Along with the insulin hormone, the patient is given small, specifically tailored amounts of glucose (ingested as a dextrose liquid) to stimulate the digestive system and its role in the metabolism process during treatment.

Each session lasts about two to three hours, and the patient is free to move around the clinic during the session.

Insulin Sensitisation – By achieving insulin sensitivity at the insulin receptor level, glucose can more readily enter cells and be converted into adenosine triphosphate, also known as ATP–a molecule that carries energy within cells.

The benefits of PIR have been known about and documented since about 2012 but the technology to apply it outside of a research lab and in a clinic environment was only developed in 2017.  A US company, Well Cell Global Inc. was the developer and is now the holder of multiple international patents covering the technology.  HealthyCells.uk has the exclusive rights for this PIR modality in the UK and Ireland.

To date, there are over 200 clinics worldwide offering PIR.  Thousands of patients have been treated and over 200,000 PIR infusions have been performed, without any side effects or adverse reactions.  More than 10 university and clinical institutions are currently using PIR in a monitored research environment.  To date, two patents for PIR have been issued and a third is pending. 

The pulsatile insulin delivery is designed to upregulate insulin receptor expression and signalling pathways, reversing or reducing insulin resistance at the cellular level.

The treatment aims to restore the body's natural ability to respond appropriately to insulin, thereby improving glucose metabolism and potentially reducing the complications associated with insulin resistance and type 2 diabetes as well as other disorders caused or worsened by damaged cells.

The rationale behind physiologic insulin resensitisation is that the constant, non-pulsatile delivery of insulin, as in traditional insulin pump therapy, may contribute to insulin resistance over time. By mimicking the pancreas' natural physiological pulsatile pattern, PIR has been shown to enhance insulin sensitivity and improve the overall management of insulin resistance and type 2 diabetes.

PIR differs from traditional insulin therapy in several key aspects:

Delivery method: PIR involves the intravenous administration of insulin in a pulsatile or oscillating pattern, typically with pulses of regular insulin delivered every 4-8 minutes. Traditional insulin therapy, on the other hand, relies on subcutaneous injections or continuous subcutaneous insulin infusion (insulin pumps), which provide a more constant insulin delivery.

By mimicking the natural physiological insulin secretion, PIR aims to copy the body's natural pulsed pattern of insulin secretion from the pancreas. This pulsatile delivery is believed to upregulate insulin receptor expression and signalling pathways, potentially reversing or improving insulin resistance at the cellular level. Traditional insulin therapy cannot replicate this natural physiological pattern.

Resensitisation to insulin: The pulsatile nature of PIR is designed and tailored to resensitise cells to insulin action by restoring the body's ability to respond appropriately to insulin. Traditional insulin therapy does not specifically target insulin resistance or resensitisation.

Concurrent glucose administration: During PIR, oral glucose is administered concurrently to maintain blood glucose levels within a therapeutic range and stimulate the body's metabolic response. Traditional insulin therapy does not involve concurrent glucose administration.

Treatment duration: A course of PIR treatment is typically administered for a limited duration, ranging from a few days to a few months, as a resensitisation therapy. Traditional insulin therapy is a long-term, ongoing treatment for managing diabetes.

In summary, PIR is a novel approach that aims to mimic the natural physiological pulsatile pattern of insulin secretion and resensitise cells to insulin action through intravenous pulsatile insulin delivery and concurrent glucose administration. This contrasts with traditional insulin therapy, which provides a more constant insulin supply without specifically targeting insulin resistance or mimicking physiological insulin patterns.

Yes.  Using an insulin pump can potentially lead to insulin resistance in some cases. 

Here's how:

• High insulin doses: Patients with type 2 diabetes often require high doses of insulin due to severe insulin resistance. When using an insulin pump, these high doses are delivered continuously and subcutaneously, leading to sustained high levels of insulin distributed around the body. Chronic exposure to high insulin levels can further exacerbate insulin resistance over time.
• Lipohypertrophy: Repeated insulin injections at the same site can cause lipohypertrophy, which is an accumulation of fat deposits under the skin. These fat deposits can impair insulin absorption and action, contributing to insulin resistance.
• Infusion set issues: If the insulin pump's infusion set becomes kinked, dislodged, or obstructed, it can lead to inconsistent insulin delivery. This erratic insulin exposure can disrupt glucose metabolism at the cellular level and potentially worsen insulin resistance.
• Injection site resistance: The subcutaneous tissue can develop resistance to the introduction of fluid, including insulin, over time. This increased tissue resistance can impair insulin absorption and action, leading to higher insulin requirements and potentially exacerbating insulin resistance.
• Weight gain: Some patients may experience weight gain while using an insulin pump, especially if insulin doses are not appropriately adjusted. Excess weight, particularly abdominal obesity, is a major risk factor for insulin resistance.
• Continuous insulin exposure: Insulin pumps deliver a continuous infusion of insulin, leading to sustained high levels of insulin in the body. Chronic exposure to high insulin levels can contribute to the development of insulin resistance over time, as cells become desensitised to the effects of insulin.
• High insulin doses: Patients with type 2 diabetes often require high doses of insulin due to severe insulin resistance. When using an insulin pump, these high doses are delivered continuously, further exacerbating insulin resistance.

However, it's important to note that the impact of insulin pump therapy on insulin sensitivity will vary among individuals and may depend on factors such as the duration of diabetes, degree of insulin resistance, and overall metabolic control.

A number of peer-reviewed clinical trials have been published.

Clicking on the QR code or on the link below will take you to a selection of these trials.

All the reports are available for download from the link.

https://wellcellglobal.com/research/

Further reports are available on request

Unfortunately not.  

Metabolic impairment is a chronic disease. If patients stop their PIR therapy, the improvements experienced from these treatments will diminish over time if other actions aren't taken.  PIR has shown itself to be extremely effective at repairing some of the damage done by diabetes, for example curing foot ulcers, preventing the need for lower limb amputations and avoiding diabetes-induced blindness, but it is not a long-term cure for the disease itself.

Our clinics will be suggesting advice and guidance on where to find diet and exercise programmes that can be used to put diabetes into remission.

While there is no known permanent cure for type 2 diabetes, extensive research shows that it is possible for some people to reverse the condition and achieve remission. Here are the key points about reversing type 2 diabetes:

Remission is defined as blood sugar levels returning to a non-diabetic range without the need for glucose-lowering medications.  The primary method for achieving remission is significant weight loss, typically 30 pounds or more.

There are several approaches to potentially reverse type 2 diabetes:

• Low-calorie diet: Studies have shown that following a very low-calorie diet (625-850 calories per day) for 2-5 months, followed by a less restricted diet, can help nearly half of participants achieve remission for at least 6 months to a year.
• Bariatric surgery: This type of weight loss surgery can lead to diabetes remission in up to three-quarters of patients, especially those who have had the disease for 5 years or less and don't use insulin.
• Lifestyle changes: Losing 7-10% of body weight through diet and exercise can improve insulin sensitivity and help manage blood glucose levels.

Remission is more likely to be achieved in people who:

• Have had diabetes for a shorter duration
• Are not using insulin
• Lose significant amounts of weight

It's important to note that remission is not always permanent, and the underlying genetic factors contributing to diabetes susceptibility remain. The disease process may reassert itself over time, especially if weight is regained.

Even if complete remission is not achieved, lifestyle changes and weight loss can significantly improve blood glucose control and reduce the need for medications.

So, to summarise, PIR is excellent at repairing some of the damage done by diabetes at the cellular level and should lead to conditions such as ulceration clearing up, so reducing the need for foot or lower leg amputations.  Longer term, though, once the damage has been repaired, diabetes can best be put into remission by following some of the excellent and proven advice that is available.  HealthyCells.uk can advise on where to find this guidance.

There is no magic pill or supplement that can cure diabetes. Experts caution against products claiming to cure diabetes or replace prescribed medications.

In other words, PIR can effectively and efficiently repair the damage done at cellular level by diabetes, and can go to greatly support and accelerate the process of putting the disease into remission by proven regimes in diet, exercise and weight loss. 

There are early-stage clinical studies currently underway designed to explore how our PIR modality can help restore health to damaged kidneys.  The results so far have been extremely positive and encouraging although we should stress that no clinical trial reports have yet been peer-reviewed. 

Kidney cells require insulin to function properly. Here are the key points about how insulin affects kidney cells:

Both insulin receptor isoforms are widely expressed in the kidney, indicating that insulin acts on all renal cell types including mesangial cells, podocytes, and tubular epithelial cells.

In the proximal tubule cells, insulin is filtered from the blood and completely reabsorbed from the tubular lumen. Insulin receptors on the basolateral membrane facilitate this uptake of insulin.

Insulin has several functions in the renal tubules, including regulating metabolism, electrolyte balance, acid-base balance, and absorption of glucose and other nutrients.

Insulin stimulates reabsorption of sodium, phosphate, and glucose in the distal nephron segments after diffusing from peritubular capillaries.

Insulin degradation also occurs in proximal tubule cells via enzymatic pathways involving insulin protease, glutamyl aminopeptidase, and lysosomal proteases.

In summary, insulin receptors are present on various kidney cell types, allowing insulin to exert metabolic effects, regulate solute and electrolyte transport, and undergo degradation, highlighting the importance of insulin for proper renal function.

We have anecdotal evidence, as yet undocumented or peer-reviewed, that our PIR modality is having a strong beneficial effect for people suffering from Alzheimer's and Dementia.

There is a proven link between diabetes and Alzheimer's disease. Multiple studies have demonstrated a strong connection between these two conditions:

People with type 2 diabetes have a significantly increased risk of developing Alzheimer's disease. Research has shown that diabetic patients have a 65% higher risk of developing Alzheimer's compared to those without diabetes.

The relationship between diabetes and Alzheimer's is so robust that Alzheimer's is sometimes referred to as "type 3 diabetes" or "brain diabetes". This terminology reflects the shared mechanisms and risk factors between the two conditions.

Long-term studies have revealed that the earlier a person develops diabetes, the greater their risk of developing dementia, including Alzheimer's disease. For instance, individuals who had diabetes for more than 10 years had a significantly higher rate of dementia compared to those without diabetes.

The link between diabetes and Alzheimer's is attributed to factors such as:

Insulin resistance in the brain cells, which can lead to impaired cognitive function and contribute to the formation of amyloid plaques, a hallmark of Alzheimer's disease.

Chronic high blood sugar levels, which can damage blood vessels in the brain and contribute to cognitive decline.

Shared risk factors such as high cholesterol, inflammation, and cardiovascular disorders.

While the exact mechanisms are still being studied, the clinical research evidence clearly shows a significant link between diabetes and an increased risk of Alzheimer's disease. We are seeing early indications that PIR can repair some of the brain cell damage suffered by these patients.  We should stress, though, that these indications are presently purely anecdotal and we can reasonably expect thorough research to take several years, owing to the long-term nature of these diseases.

We have anecdotal evidence, as yet undocumented or peer-reviewed, that the PIR modality is having a strong beneficial effect for people suffering from Parkinson’s Disease, specifically the 'facial mask' and shuffling gait syndromes that can be seen in early-stage Parkinson's sufferers. 

There is evidence suggesting a link between diabetes and Parkinson's disease (PD). Several studies have investigated this connection, revealing the following key points:

Increased risk: People with type 2 diabetes have a higher risk of developing Parkinson's disease. A meta-analysis of seven observational cohort studies found that patients with type 2 diabetes had a 38% increased risk of developing PD compared to non-diabetic individuals.

Shared mechanisms: Both diabetes and Parkinson's disease share some common pathophysiological mechanisms, including insulin dysregulation, oxidative stress leading to mitochondrial dysfunction, microglial activation, and inflammation.

Insulin's role in the brain: Insulin plays a crucial role in neuronal survival and brain function. Changes in insulin metabolism and signalling in the central nervous system can contribute to the development of various brain disorders, including PD.

Insulin resistance: A large proportion of people with Parkinson's, even those without diabetes, show reduced responsiveness to insulin. This has led to ongoing research into understanding the role of insulin and glucose in PD.

However, there is still some conflicting evidence: While cohort studies consistently show diabetes as a risk factor for future PD, case-control studies have not proved an association between diabetes and PD prevalence. This discrepancy might be due to decreased life expectancy in patients with both conditions or selection bias in case-control studies.

It's important to note that while there is a link between diabetes and an increased risk of Parkinson's disease, having diabetes does not necessarily mean a person will develop PD. The relationship between these two conditions is complex and continues to be an active area of research.  As has been mentioned above, the evidence of improvement in early-stage PD patients undergoing our PIR therapy is still anecdotal and as yet untested in a controlled clinical trial environment.