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Bones could be your solid allies in fighting diabetes
One important breakthrough in medical research in the past few years has been the reclassification of bone as a hormone-secreting endocrine organ. With this, our traditional understanding of the bone’s identity has undergone a drastic reboot.
This development could open new frontiers to learn about, tackle and manage diabetes.
It would be ironic today to keep using the term skeletal in its literal context while referring to our bones.
One important breakthrough in medical research in the past few years has been the reclassification of bone as a hormone-secreting endocrine organ. With this, our traditional understanding of the bone’s identity has undergone a drastic reboot.
It has been revealed that the skeletal system is not merely a framework of bones, cartilage and ligaments that supports, shapes and makes us mobile. It has been pointed out that the bones are literally chatterboxes involved in constant crosstalk with other organs and directly influencing multiple life processes (including glucose metabolism).
Say hello to osteocalcin
The key player here is osteocalcin, mainly its undercarboxylated form, a bone hormone secreted during bone-cell remodelling that has been shown to interact with pancreas and favour insulin secretion and better glucose absorption.
This triggered a cloudburst of activity in the field of bone endocrinology since the last decade involving top researchers including Dr Gerard Karsenty, professor and chair of the Department of Genetics and Development, Columbia University Medical Centre, New York City. Their main objective: to unravel the dynamics of this insulin-bone pathway in our cells so that it could be enhanced through targeted therapeutic intervention to tame the global epidemic of type 2 diabetes.
“Osteocalcin has several functions related to glucose homeostasis. It favours insulin secretion by pancreatic beta cells; second is that it favours glucose uptake at least in muscle and possibly in other tissues,” Prof Dr Karsenty told Happiest Health in an online interaction. Homeostasis is a state of equilibrium or balance between multiple components involved in physiological processes in our body.
Dr Karsenty said osteocalcin also favours gluconeogenesis in the liver, which sort of counterbalances any possibility of hypoglycaemia (low blood glucose levels) in the body due to additional insulin secreted through this loop. During gluconeogenesis the liver processes and release additional glucose, mainly from non-carbohydrate sources.
Dr Karsenty is credited as the first researcher to have discovered osteocalcin’s role in glucose metabolism back in 2007.
However, it took a couple of years more for his research team to finally announce in 2010 that the new insulin pathway of undercarboxylated osteocalcin, pancreatic beta cells, insulin and also adipose tissues could play a pivotal role in balancing our blood glucose levels and body weight management.
In a media release at that time, Columbia University had said that stimulation of the bone-insulin pathway could lead to a better cure or management strategy for type 2 diabetes in the future.
“This feed forward loop is only between osteoblasts that makes osteocalcin and pancreatic cells that make insulin,” Dr Karsenty told Happiest Health. “Osteocalcin favours insulin secretion and insulin favours secretion of bioactive osteocalcin (undercarboxylated).”
Welcome to the bone matrix
Bones are perhaps the most dynamic organs of the body — appearing inert but yet caught in a constant chaotic state of modelling and remodelling to ensure that they could keep pace and adapt to various physiological changes and trauma as people age on in life.
This is basically ensured by the death of old bone cells to get re-absorbed into the blood (resorption) and simultaneous formation of new bone cells to replace these old cells. Our bones are generally made up of a calcium-rich intercellular bone matrix and three types of cells (osteoblasts, osteoclasts and osteocytes).
- osteoblasts, which are responsible for bone formation
- osteoclasts are the ones for bone resorption
- osteocytes, which are mainly a variant of osteoblasts involved in sensory functions pertaining to bone formation and remodelling
“Osteocalcin is a protein hormone predominantly released by osteoblasts (responsible for bone synthesisation and mineralisation) and physiologically plays an important role in bone formation and remodelling,” Prof Dr Antonio Brunetti, professor of endocrinology, University of Magna Graecia of Catanzaro and director of Operative Unit of Endocrinology, AOU Mater Domini, Catanzaro, Italy, told Happiest Health in an online interaction. “Recent studies have shown that osteocalcin is also involved in other important processes not directly linked with bone physiology, such as regulation of whole-body glucose metabolism.”
Osteocalcin is in fact one of the most abundant bone protein hormones in the intercellular bone matrix. Osteocalcin was always considered as a marker and agent of osteoblastic bone formation, but it was only after researchers started to look closer at this hormone that it became evident that bone formation could actually be just one of the many functions of this dynamic hormone. It was soon found that osteocalcin is actually an undercover endocrinal agent embedded in the bone matrix involved in an array of physiological function including glucose metabolism and even energy expenditure, ageing and cognitive abilities.
“The endocrine function of osteocalcin appears to be primarily related to its under-carboxylated form, and to a lesser extent to its carboxylated form, but the available scientific evidence in this context is conflicting,” said Prof Dr Brunetti. “Regardless of the osteocalcin carboxylation state, investigations from our own group and others have shown that elevated blood glucose concentrations (hyperglycaemia) in patients with diabetes are consistently associated with low circulating levels of osteocalcin. Indeed, there is a suggestion that this bone-derived hormone, either directly or indirectly, stimulates the production and release of insulin by pancreatic beta cells. In normal conditions, insulin helps to ensure that blood glucose is taken up by the liver, adipose tissue and skeletal muscle after a meal, preventing high blood glucose peaks.”
Loop before you leap
Prof Dr Mathieu Ferron, director of the Molecular Physiology Research Unit at the Montreal Clinical Research Unit (ICRM) and associate research professor and Canada Research Chair in Bone and Energy Metabolism at the ICRM, told Happiest Health in an online interaction that there was an insulin receptor located on osteoblasts and some of the initial research work on osteocalcin and glucose metabolism involved removal of these insulin receptors from specially bred lab mice. Prof Ferron was also part of the team that Dr Karsenty led in 2010 when they officially pointed out the link between bones, glucose uptake and insulin secretion.
“Our data (Ferron 2010, Cell) suggest that osteocalcin stimulate insulin production, and that in return insulin acts on bone to promote osteocalcin release,” Prof Dr Ferron said. “We observed that the insulin receptor is present on osteoblasts. Removing insulin receptor specifically in this cell type resulted in surprising effects in mice: they had more fat, less insulin and higher blood glucose. We also found that serum osteocalcin was reduced in these animals. In other words, insulin through its action on bone regulates whole body glucose level! Through a series of studies we next established that insulin stimulates not only osteoblast to produce more osteocalcin, but also osteoclasts, the bone-resorbing cells, which is responsible of decarboxylating and activating osteocalcin.”
Interestingly, it has been pointed out that Dr Karsenty and his team was trying to unravel the role of osteocalcin in bone formation and decided to experiment after removing the gene responsible for osteocalcin when they realised that it did not have a serious impact on the bone formation, but the mice soon became obese, glucose intolerance and also started showing symptoms of cognitive impairment.
Further research by their team revealed that bone resorption was integral to the completion of this feed forward loop as regular carboxylated osteocalcin changes into under carboxylated form as a direct result of high acidic conditions caused due to bone resorption by osteoclasts and sets up this feed forward loop in motion.
“In addition to these correlative studies a few articles have reported that human osteocalcin can impact human beta cell function in a petri dish (in vitro) or in a diabetic mouse transplanted with human beta cells (in vivo),” Dr Ferron said.
Dr Ferron said there are about 100 cross-sectional studies in humans which show that higher level of osteocalcin in the blood are associated with lower glucose or that lower osteocalcin is associated with higher risk of diabetes.
“In support of this view, recent in vitro experiments from our lab have highlighted that exposure to conditioned medium from human MG-63 osteoblasts*, which are low in osteocalcin content because of an impaired insulin receptor signalling, can actually reduce the insulin-producing response of cultured pancreatic β-cells to glucose stimuli,” Prof Dr Brunetti said. (*MG 63 osteoblasts area-specific human osteoblast like cells used for lab experiments).
In a joint response to Happiest Health, Prof Dr Brunetti along with his colleagues Dr Maria Mirabelli and Dr Alessandro Salatino from the University of Magna Graecia said, “In fact, according to current research, obese individuals who are insulin resistant have a different pattern of secreted adipokines than people who are not obese. The past few decades have also witnessed an extensive disentangling of the insulin receptor signalling pathway, with the identification of non-canonical insulin target tissues that appear to play an important role in whole-body glucose homeostasis, including the bone.”
They also pointed out that the adipose-bone and pancreas axis of osteocalcin will be deeply impaired in obese people and those with diabetes as they would be already affected by insulin resistance leading to high blood sugar levels.
Better diabetes management options?
One of the main obstacles that researchers had to face while trying to enhance the effect of osteocalcin in humans was to ensure that it could stay longer in our blood stream without being broken down by enzymes. It was found that osteocalcin in mice was always five to 10 times higher than in humans.
In 2020 a group of researchers including Prof Dr Ferron published their research stating that osteocalcin in mice was more stable than that in humans because it has a group of sugars attached to its protein structure, which is not present in human osteocalcin. Researchers are now working on modified human osteocalcin that could be maintained at high levels in our blood without getting filtered out by the kidney or broken down by enzymes.
The potential of the ongoing research into osteocalcin’s blood sugar regulatory role could be gauged to an extent from the fact that Prof Dr Ferron’s work on osteocalcin, ‘A hormone produced by bone to treat Diabetes’, was adjudged as one among the 15 diabetes-related research projects from across the world to be bestowed with the End Diabetes: 100 Awards in 2021. Constituted by the Canadian Diabetes Association, the award carries an annual grant of $100,000 for three years. Last year was also the centennial anniversary of the discovery of insulin by Dr Frederick Banting, Dr Charles H Best and JJR Macleod in Toronto.
“My lab is currently working on a modified human osteocalcin protein that is more stable in the blood, with the goal of using it as a new therapeutic approach for diabetes,” Prof Dr Ferron said. “Osteocalcin is a protein produced in bone tissue that travels to our pancreas, fat and muscles to regulate blood glucose. Harnessing the specialized function of this protein could become a ground-breaking treatment for type 2 diabetes.”
Happiest Health also posed the question about osteocalcin’s role in diabetes management in the near future to Prof Dr Karsenty. He confirmed that his team was also working on a project to ensure better management of blood sugar using this bone hormone.
Dr Tom Babu, medical director, consultant diabetologist and endocrinologist, Silverline Hospital, Kochi, Kerala told Happiest Health that it was fascinating that the bone is being now considered as an endocrine organ. He said it holds promise for therapeutic interventions in the future and more research is being carried out in this direction.
“I would definitely keep watching this space,” Dr Babu said. “In my clinical practice I have seen that people with better bone health seem to be better placed with regards to metabolic diseases.”
Bone-sigh: Manage glucose levels to deal with osteoporosis
Simply put, osteoporosis is the gradual weakening of the bones, putting them at a higher risk of fracture and related complications. People with diabetes may also have various vascular and neurological conditions, affecting their balance. Elderly people with diabetes are therefore advised to protect themselves from falls and injuries
Thirty-year-old private school teacher Sini’s (name changed on request) prime concern apart from her professional and personal commitments is the well-being of her 83-year-old diabetic mother. A resident of Kochi in Kerala, Sini’s mother however continues to remain active for her age but has had diabetes for over three decades. Her mother suffered a heart attack about six years ago after the sudden demise of her father.
“In a way, my mother is quite healthy for her age, and she insists on doing all her chores by herself which is a bit scary for me. We always keep telling her to be careful and mindful whenever I step out to go to school. She is on medication for diabetes and was put on pills after her heart attack. Our doctor had also prescribed her calcium supplement tablets. Anyway, thankfully we keep a close watch over her blood sugar levels through periodic checkups and personal care,” Sini says. She points out that her mother became diabetic post her treatment for an intense bout of asthma but also adds that of late she has been maintaining healthy blood sugar readings. But the family always try to ensure that she doesn’t fall and suffer any bone injury especially due to her age and history of diabetes which puts her in the high-risk category for fracture and frailty-related complications.
Osteoporosis and the risk of suffering bone injuries and fractures could be one of the most worrying concerns of both the elderly and their loved ones, especially if the former has a history of fluctuating blood sugar levels.
“In general, senior citizens are more prone to bone frailty and osteoporosis. This is exaggerated in people with diabetes. The general recommendation is that women above 65 years and all post-menopausal women irrespective of age should get a bone density test done. In men generally, the testing is recommended in those above 70 years,” says Dr V Mohan, chairman and chief diabetologist, Dr Mohan’s Diabetes Specialities Centre, Chennai, in an online interaction with Happiest Health.
Diabetes and osteoporosis
Diabetes and osteoporosis are believed to be closely linked to each other. Osteoporosis could be defined in the simplest terms as the gradual loss of bone strength making the individual’s bone weak and susceptible to a higher risk of fracture and related complications. Those with chronic diabetes could also be suffering from various vascular and neurological impairments which could easily lead them to lose their balance and suffer a fall. This is one of the prime reasons why elderly people with diabetes are often advised to take extra precautions and protect themselves from falling and injuring themselves.
One of the main causes of osteoporosis is attributed to be an anomaly in the bone matrix where osteoblasts, the cells responsible for bone formation lag behind osteoclasts, the bone responsible for bone resorption (osteoclasts are responsible for the death of old bone cells and its assimilation into the bloodstream as new bone cells replace them). In people diagnosed with osteoporosis, the rate of bone formation will be less than that of bone death which results in the overall weakening of the bone.
“Diabetes primarily affects the biomechanical properties of the bone by deteriorating its organic composition and bone material strength. This occurs either directly through altered cross-link formation or indirectly through changes of cellular activity in osteoblasts and bone progenitor cells (cells with the ability to self-renew and form specialised cells),” says Dr DM Mahesh, consultant, endocrinology, Aster CMI Hospital, Bengaluru.
Thus, in people with diabetes, the blood glucose variations and its vascular comorbidities tend to scuttle the functioning of osteoblasts and other bone tissues and cells involved in bone strengthening and mineralisation. The effective functioning of bone-forming cells osteoblasts could get hampered in diabetics due to the fluctuations in the release of cytokines (proteins secreted by cells that play a major role in interactions and communications between cells) and free fatty acids from the hypoxic adipose tissue, which upholds a vicious cycle of chronic inflammation and inhibits osteoblastic activity.
“These changes eventually affect the tensile strength and post-yield properties of the bone, which make the bone tissue in people with diabetes more vulnerable to microdamage accumulation, fragility fractures at most skeletal sites and impaired fracture healing due to vascular deficiencies at the fracture site,” adds Dr Mahesh.
Dr Antonio Brunettti, professor of endocrinology, department of health sciences, University of Magna Graecia and director of the operative unit of endocrinology, AOU Mater Domini, Catanzaro, Italy, in an online interaction with Happiest Health, notes that the overall risk of fragility fractures in people with type 2 diabetes is less pronounced than in people with type 1 diabetes. He also highlights the differences in the nature of fractures in both cases.
“There are differences in the preferential location of fractures with respect to patients with type I diabetes where hip, vertebrae and distal forearm fractures are predominant as against proximal forearm and ankle fractures in those with type 2 diabetes,” says Prof Dr Brunettti. He points out that these differences could be attributed to the diverse body weight and composition of those with type 2 diabetes who are often obese and exert greater pressure and force on the ground and bones while they move around.
Dr Heather Hofflich, professor of medicine, clinical medical director, division of endocrinology and internal medicine, UC San Diego Health, tells Happiest Health in an online interaction that, based on clinical trials, there is a risk of fractures in people with both type 1 and type 2 diabetes. “However, this mechanism is complex and has not been sorted out as of yet. Therefore, it is important to check DEXA scans (to assess bone density) in both males and females with type 1 or 2 diabetes over the age of 50,” she adds.
She also notes that the only ‘extra’ precautions would be to educate anyone with diabetes on fall prevention/osteoporosis prevention mechanisms at an earlier age than the general population. She also elaborates on the osteoporosis support groups at UC San Diego Health and also the national osteoporosis support group in the US called Bone Health and Osteoporosis Foundation (BHOF) which allows people from across the United States to access information and resources on osteoporosis.
The vitamin D factor
Dr Mohan points out that vitamin D deficiency especially in those with diabetes could be one of the main connecting links between poor bone health and diabetes. He also points out that elevated blood glucose leads to chronic inflammation which adversely affects bone mass, mineral density and bone strength.
“People with diabetes are known to have low vitamin D levels. Vitamin D helps to absorb calcium, which is needed to maintain bone density. Elevated blood glucose leads to chronic inflammation which can affect bone mass, mineral density and bone strength. This can occur both in people with type 1 and type 2 diabetes. However, it is more common in people with type 2 diabetes, because type 2 diabetes occurs in older people, whereas type 1 diabetes invariably occurs in younger people,” he says.
Tips for people with diabetes, osteoporosis
- Blood sugar control
- Increasing physical activity and weight-bearing workouts
- Eating nutritious food with increased protein intake
- Maintaining healthy vitamin D and dietary calcium levels
- Restricting the intake of alcohol and avoiding tobacco in any form
Prediabetes? Here’s what you should (and should not) do
Catching a condition early is almost always an advantage, but more so when it can be checked or restrained successfully.
Prediabetes is a state in which the blood sugar levels are above the normal range, but below the range of diabetes. It is also called ‘intermediate hyperglycaemia’ or ‘high-risk state of developing diabetes’ to emphasise that measures must be taken at this stage to prevent it from progressing.
If diagnosed with prediabetes, diabetes isn’t far off, but it doesn’t have to be inevitable. “With poor lifestyle, [people with prediabetes] can become diabetic in just two months,” says Dr Tharanath S, general physician at MS Ramaiah Memorial Hospital, Bengaluru. “People may not become diabetic if they follow a very good lifestyle in terms of both diet and physical activity.”
Insulin resistance
Insulin is a hormone in the pancreas made within beta cells. After having a meal, the sugar level in the blood rises. The beta cells in the pancreas then release insulin to help the body store blood glucose.
When the cells in the body don’t respond well to insulin and can’t store the glucose, the pancreas releases more insulin to compensate for the cells’ weak response. In the case of type-2 diabetes, the insulin pumped into the blood is not enough to overcome the cells’ weak response. So, more glucose remains in the blood and isn’t stored by the body’s cells, leading to a state of high blood sugar. This is known as insulin resistance.
Type-2 diabetes is not a condition that develops suddenly; it progresses in stages. In the first stage, insulin is secreted in the body at an increased rate due to insulin resistance. The second stage is the stable adaptation period where the beta cells can’t compensate for the increased insulin resistance any more.
“Resistance is at the initial level [in prediabetes] and not as much as in full-blown diabetes. That’s why lifestyle and weight loss play a greater role in prediabetes. By burning the fat cells, insulin resistance reduces,” says Dr Tharanath.
Both stages take place before the state of prediabetes is reached. Prediabetes begins when glucose levels in the body start increasing rapidly because of insulin resistance. This is the third stage, which continues till the condition progresses to diabetes.
Symptoms and risk factors
On the outside, however, prediabetes does not have any symptoms. Even in the case of diabetes, apart from the osmotic symptoms of polyuria (increased urine), increased thirst, increased eating and weight loss, around 80 per cent of people diagnosed with diabetes are asymptomatic, says Dr Tharanath. “Because it gets picked up in a routine health check-up, we advise anybody with a strong family history to get a screening done every year. Otherwise, prediabetes doesn’t necessarily have any other symptoms,” says Dr Tharanath.
However, there are risk factors (such as obesity, genetic factors and a history of gestational diabetes) along with combinations of risk factors (like metabolic disorders) which help people remain vigilant in taking care of their bodies while getting health check-ups regularly.
“Obesity is related to insulin resistance and diabetes is a condition characterised by insulin resistance. The moment you gain weight and the moment your lifestyle is off track, you will attract type-2 diabetes. So, you need to focus on insulin resistance,” says Nidhi Nigam, a Bengaluru-based certified nutritionist and dietitian.
Lifestyle changes
A 2021 study found that more people regressed to normal glucose levels compared to those who progressed to diabetes. The stage of prediabetes is an opportunity to make changes in lifestyle and return to normal blood sugar levels.
Nigam recommends a diet rich in protein, fibre and complex carbohydrates while avoiding simple carbohydrates, processed food and junk food.
A comprehensive plan to reverse prediabetes involves the acronym ‘LEAN’. “It has four aspects – lifestyle, exercise, attitude and nutrition. Attitude is very important. You need to make sure that you don’t consider it a disease but a metabolic lifestyle disorder. Then, it can be reversed,” says Nigam.
The ‘right’ plate could be divided into four slices/quarters:
- raw vegetables
- cooked vegetables
- proteins
- complex carbohydrates (includes substituting white polished rice with brown rice, using millets, quinoa and whole wheat)
“Whatever you eat eventually gets converted into glucose, into carbohydrates. 1ml of insulin is equal to 15gm of carbohydrates. You must calculate carbohydrates accordingly,” Nigam says. It’s best to minimise the intake of sugar, she adds.
Dr Tharanath recommends avoiding junk food, red meat and high-glycaemic food. “Thirty minutes of physical activity every day is a must. This is a simple physical activity of moderate intensity,” he says.
Other than diet and exercise, lifestyle changes also include being hydrated, managing stress and getting sufficient sleep. “With this, you can not only reverse your diabetes but also achieve other health goals,” Nigam says.
Black patches: the warning bells
Acanthosis Nigricans (AN) is an odd name. However, this medical condition isn’t new to many. A disorder characterised by dark, thick patches on the skin-fold regions like the axilla, groin and back of the neck, is most frequently linked to diabetes and insulin resistance. It can also occasionally be an indicator of internal malignancy. Sometimes, it can be caused by drugs too, like oral contraceptives or systemic glucocorticoids – anti-inflammatory drugs that work with the immune system to treat a wide range of illnesses.
This condition typically affects people under 40. It may be genetically inherited or linked to obesity, hypothyroidism, polycystic ovary syndrome (PCOS) and insulin resistance. Because of unhealthy lifestyle patterns and related complications, insulin resistance and prediabetes have emerged as the main reason for people to develop this condition.
Bibin J E, a 38-year-old quality health safety and environment project co-ordinator with a private oil and gas firm in the United Arab Emirates who weighed 136 kgs and was suffering from a horde of adverse lifestyle health conditions, including high blood sugar levels, tells Happiest Health how he developed black patches near his neck. It was one of the initial signs that forced him to seek medical help and realise that he was at serious risk of developing type 2 diabetes. However thankfully motivated by his doctor’s advice and his determination to lose weight, he managed to bring down his body weight and also avert the looming threat of diabetes.
The American Diabetes Association has formally recognised AN as a predictor of the development of diabetes. The condition is more common in Native Americans, African Americans and Hispanics than in people of white or Asian origin in the United States.
According to Dr Vijay Viswanathan, head and chief diabetologist, MV Hospital for Diabetes and Research Center, Chennai, AN is a skin marker for insulin resistance. “The condition in which the folds such as the armpits and nape of the neck become more pigmented could result in type 2 diabetes,” confirms Dr Viswanathan, one of the veteran diabetologists and researchers in South India.
Insulin resistance, a condition in which insulin doesn’t work as well as it should, is a sign of the most common type of AN. Insulin, a hormone produced by the pancreas, controls the amount of glucose in the blood by making glucose move into cells to make energy or into the liver and fat cells to store energy. The main source of energy for cell metabolism in the body is glucose, which is a simple sugar. AN is thought to be caused by a build-up of insulin in the blood, which is caused by insulin resistance. Insulin resistance has been linked to several diseases, including obesity, polycystic ovary syndrome (PCOS) and type 2 diabetes.
When insulin resistance is the most frequent cause of AN in children and young adults, basal and glucose-stimulated insulin levels are higher in children with AN compared to obese children without the condition; this is linked to hyperinsulinemia (the amount of insulin in the blood is higher than what’s considered normal) independently of body mass index.
According to studies from both India and the United States, there is a clear connection between Acanthosis Nigricans and childhood obesity. Regular and adequate physical activity can help to delay the onset of the condition. The high prevalence of AN in women with diabetes is known to be partly or entirely due to PCOS, an insulin-resistant condition.
The build-up of insulin in the blood explains why the body converts carbohydrates into glucose when we eat. While the body stores the remaining glucose, cells use some of it for energy. For cells to use glucose as energy, the hormone insulin must permit glucose to enter the cells. People who are overweight tend to develop resistance to insulin over time. Although the pancreas produces insulin, the body has trouble effectively using it. This causes a build-up of glucose in the blood, which may result in high levels of glucose and insulin in the blood.
Dr Nihal Thomas, professor and head of the department, endocrinology, diabetes, and metabolism, Christian Medical College in Vellore, talks about the different types of Acanthosis Nigricans. She says that type 3, also referred to as obesity and pseudoacanthosis nigricans, is a very prevalent form. “If the underlying causes, such as insulin resistance, obesity, etc, are treated, this may lessen and even go away. But this may take months or years. Type 1 acanthosis can appear at birth or develop during childhood and is brought on by an autosomal dominant trait. Type 2 AN is related to diabetes and metabolic syndrome. Type 4 Acanthosis Nigricans is linked to the use of oral contraceptives and growth hormone therapy,” he says.
Benign forms of the condition commonly manifest during childhood or puberty. Benign Acanthosis Nigricans, which occurs less commonly, may be present at birth or develop after puberty. The latter cases almost always involve Acanthosis Nigricans in conjunction with obesity (pseudoacanthosis nigricans).
Malignant Acanthosis Nigricans, usually appears after the age of 40. Experts believe that several factors may point to malignant Acanthosis Nigricans in combination with underlying cancer. These include adult-onset symptoms that are unrelated to the use of specific medications, obesity, positive family history and certain underlying disorders known to be associated with the condition. On rare occasions, malignant Acanthosis Nigricans can develop in children.
The condition can be reversed and will go away in six to eight months if the person adopts healthy lifestyle habits, says Dr Thomas. Hereditary variants may or may not fade with age, and malignancy-associated variants may fade after a malignancy is removed.
“On the subject of treatment, endocrine-related Acanthosis Nigricans can be managed by reducing blood sugar levels through diet and exercise. Selenium sulfide-containing creams are used to treat the condition. The causative tumour can be removed to treat malignant Acanthosis Nigricans. However, it is certain that it can be reversed in a number of scenarios; it may go away if the underlying causes are treated. If it is drug-induced, it disappears when the drug is stopped. Weight loss also helps with obesity-related Acanthosis Nigricans,” says Dr Thomas.
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Very usefull