Retha Harmse explores the intricate relationship between antidepressants and blood glucose regulation.

Listen to this article below or wherever you get your podcasts or visit our playlist.

Antidepressants are indispensable in treating various mental health disorders, such as depression, anxiety, and obsessive-compulsive disorder. Given their widespread use, understanding their potential effects on physiological processes, particularly blood glucose regulation, is crucial for optimising patient care. In parallel, maintaining stable blood glucose levels is fundamental for overall health and well-being.

Antidepressants operate through different classes, each with distinct mechanisms of action. Understanding these classes’ nuances is pivotal for gauging their impact on blood glucose regulation and metabolic health.

• Selective serotonin reuptake inhibitors (SSRIs) increase serotonin levels by impeding its reuptake, enhancing mood.
• Tricyclic antidepressants elevate both serotonin and norepinephrine levels, albeit with more side effects.
• Atypical antidepressants encompass a heterogeneous group targeting various neurotransmitter systems to alleviate depressive symptoms.

The mechanisms through which antidepressants influence blood glucose levels are multi-faceted. They may directly affect glucose metabolism via interactions with insulin signalling pathways or modulate the hypothalamic-pituitary-adrenal axis, impacting insulin sensitivity.

Furthermore, changes in lifestyle factors, such as diet, exercise, and stress levels induced by antidepressants, can indirectly influence blood glucose regulation. By clarifying these mechanisms, researchers aim to inform clinical practice and enhance patient management strategies.

Research insights

Research investigating the effect of antidepressants on blood glucose levels has yielded valuable insights. Clinical trials, longitudinal studies, and mechanistic research have provided evidence of inter-drug variability and individual responses among diverse patient populations.

Such findings underscore the importance of tailored treatment approaches and highlight the need for further research to explain underlying mechanisms and identify personalised interventions.

Clinical implications of antidepressant treatment on blood glucose regulation are profound. People with diabetes or predisposition to diabetes require meticulous screening and monitoring, emphasising interdisciplinary care to optimise treatment outcomes and mitigate metabolic risks. Regular blood glucose monitoring throughout antidepressant therapy, coupled with patient education, and lifestyle modifications, forms the cornerstone of effective management.

Strategies for managing potential effects on blood glucose

1. Lifestyle modification

Healthy lifestyle behaviours, including regular physical activity, balanced nutrition, and stress management, can help mitigate potential metabolic effects of antidepressant treatment.

2. Medication adjustment

In some cases, medication adjustments may be necessary to address changes in blood glucose levels, such as switching to an antidepressant with a more favourable metabolic profile or adjusting concurrent diabetes medications.

3. Individualised approach

Tailoring treatment plans to the unique needs and characteristics of each patient, including their psychiatric and medical history, can optimise outcomes while minimising metabolic risks.

4. Nutritional counselling

Dietary counselling tailored to the person’s needs, emphasising balanced nutrition and monitoring carbohydrate intake is advised. Registered dietitians can offer personalised meal planning to help stabilise blood glucose levels.

5. Physical activity promotion

Regular physical activity is encouraged as part of a holistic approach to managing blood glucose levels. Physical exercise can improve insulin sensitivity and glucose uptake, potentially counteracting any adverse metabolic effects of antidepressant treatment.

6. Stress reduction techniques

Practise stress reduction techniques, such as mindfulness meditation, deep breathing exercises, or progressive muscle relaxation. Chronic stress can contribute to glucose dysregulation, so managing stress effectively may help mitigate potential metabolic effects of antidepressants.

7. Regular follow-up and monitoring

Schedule regular follow-up appointments to assess treatment response and monitor changes in blood glucose levels over time. Adjust treatment plans as needed based on clinical outcomes and laboratory data.

8. Sleep hygiene practices

Good sleep hygiene is needed for adequate sleep duration and quality. Poor sleep habits can disrupt glucose metabolism and exacerbate metabolic disturbances associated with antidepressant use.

9. Pharmacogenomic testing

Consider pharmacogenomic testing to identify genetic variations that may impact an individual’s response to antidepressant medications. Tailoring treatment based on genetic factors can optimise efficacy while minimising adverse metabolic effects.

10. Patient education and empowerment

Empower patients with knowledge about the potential effects of antidepressants on blood glucose levels and equip them with self-management strategies. Encourage proactive engagement in their healthcare by monitoring symptoms, adhering to treatment plans, and seeking assistance when needed.

Comprehensive patient care

The intricate interplay between antidepressants and blood glucose regulation underscores the importance of comprehensive patient care. By integrating knowledge of antidepressant mechanisms, research findings, and clinical implications into practice, healthcare providers can optimise treatment strategies while safeguarding metabolic well-being.

Further research endeavours are essential to advance the understanding and refine personalised interventions, ultimately enhancing patient outcomes in mental health care.

Header image by FreePik

Dr Paula Diab lists the wonders of the new advancement of ultra-rapid insulin and who would benefit from using it.

Listen to this article below or wherever you get your podcasts or visit our playlist.

To get a good understanding of what ultra-rapid insulin is and does, it’s best to get a broad overview first; and for that, we need to take a step back in time.

Early discoveries

Insulin was first discovered in the early 20^th century. Before then, diabetes was a fatal disease due to the inability to control blood glucose levels.

In 1921, a breakthrough occurred when Canadian scientist Frederick Banting, Charles Best, along with John Macleod and James Collip, successfully isolated insulin from the pancreas of dogs. This discovery earned Banting and Macleod the Nobel Prize in Physiology or Medicine in 1923. The first human patient was treated with insulin in 1922, transforming diabetes from a fatal diagnosis to a manageable condition.

Evolution of insulin types

Over the years, various types of insulins became available. Initially, porcine and bovine insulins were produced; these remained in use until about the 1980s. These insulins were extracted from the pancreases of pigs or cows and although effective, did sometimes cause allergic reactions due to slight differences from human insulin.

During the 1980s, recombinant DNA technology revolutionised insulin production, where scientists were able to reproduce human insulin in the laboratory. This reduced allergic reactions and improved efficacy.

Insulin analogues became available from the 1990s. These are synthetic insulins that have been genetically engineered to alter the structure of the hormone, allowing for improved pharmacokinetic properties compared to regular human insulin. These modifications help to better mimic the body’s natural insulin response, making them more effective in managing blood glucose levels in people with diabetes.

Duration of action of insulin

Apart from the different types of insulin, it can also be categorised according to its duration of action.

• Rapid-acting insulins: Insulin lispro, insulin aspart, and insulin glulisine all start working within 10 – 20 minutes, making them suitable for controlling blood glucose spikes during meals.
• Short-acting insulins: Regular human insulin remains in use in some countries for managing mealtime blood glucose and acts within 30 minutes. It can be particularly useful if you want a slightly delayed and extended response to the meal.
• Intermediate-acting insulins: Neutral protamine Hagedorn (NPH) insulin, introduced in the 1940s, acts within one to two hours and is sometimes still used for basal insulin needs, although it does still have peaks and doesn’t last the full 24 hours.
• Long-acting insulins: Long-acting analogues like insulin glargine and insulin detemir, introduced in the early 2000s, provide a steady insulin level over 24 hours, reducing the number of injections needed and providing much more predictable and reliable control than the old human insulin counterparts. This is the basis of insulin therapy for most people.
• Ultra-long-acting insulins: Newer ultra-long-acting insulins, such as insulin degludec, last up to 42 hours, offering even more flexibility and convenience.

Figure 1: Duration of action of insulins. (Insulin_short-intermediate-long_acting.png: Anne Peters, MDderivative work: M•Komorniczak -talk-, CC BY 3.0 https://creativecommons.org/licenses/by/3.0>, via Wikimedia Commons).

It’s important to note from Figure 1 that each insulin may peak at the time suggested but this may vary amongst individuals. It’s also important that many insulins still remain active within the body for some time and even short- and rapid-acting insulin may take six to 10 hours to be completely eliminated from the body.

Structure of insulin therapy

Long-acting insulin usually forms the basis of insulin therapy for most people. This will give a constant background amount of insulin throughout the entire day. In some cases, this dose may need to be given as a divided dose but generally it’s given as a single injection either in the morning or evening.

The purpose of long-acting insulin is controlling your fasting glucose levels (the first reading you take in the morning). Once these levels are stable and in range, you can begin to look at what additional medication may be required. This is where an individualised approach to diabetes management becomes so important.

The treating clinician will weight up the individual risk factors, various lifestyle constraints, and other practical influences to determine what is best recommended. These days there are many options, from oral therapy (drugs that fall into the classes of sulphonylureas, SGLT2 inhibitors, DPP4 inhibitors) to other types of injections (drugs that fall into the class of GLP1 agonists), or mealtime insulin.

Mealtime insulin

The purpose of mealtime insulin is to provide a balanced insulin response to the food that you eat at each meal. Very few of us, if any, eat exactly the same food for every meal, every day.

Mealtime insulin needs to be adjusted depending on multiple factors and given at a distinct time before the meal for it to work at its optimum. Ideally the calculation should include an assessment of the carbohydrates in the meal although the protein and fat content may also need to be considered.

The pre-meal glucose value is also important as is information on whether the glucose levels are rising or falling prior to the meal. There are many factors that influence this calculation but, in most cases, we tend to get away with a well-determined educated guess and adjust from there. Insulin pumps do a much better job of calculating this dose more accurately and giving more precise doses.

As opposed to the basal dose of long-acting insulin which is given once a day in the same dose every day, mealtime insulin is usually rapid- or short-acting insulin. These insulins have the ability to work much quicker within the body and provide insulin in response to the meal.

The main problem with rapid or short-acting insulin is that their response time is still slower than the time it takes for glucose to be absorbed from the meal. For this reason, clinicians often suggested taking insulin slightly before the meal to counter-act this delay but this is often not practical. Sometimes, the timing of the meal may not be accurate, such as in restaurants, the content of the food may not be known, or the person may not finish the entire meal, as often happens with children or the elderly. 

Ultra-rapid insulin: A game changer in diabetes management

The most recent development in the insulin family is the ultra-rapid insulins such as aspart and insulin lispro-aabc. These insulins start working in about two to five minutes, closely mimicking the body’s natural insulin response to meals. This rapid onset is achieved by adding ingredients that speed up absorption into the bloodstream. For instance, aspart includes vitamin B3 (niacinamide) and an amino acid (arginine), which enhances its speed of action.

What are the benefits of ultra-rapid insulin

1. Better post-meal blood glucose control

Ultra-rapid insulin works quickly enough to match the rapid rise in blood glucose levels that occurs after eating. This helps to keep blood glucose levels more stable and reduces post-meal spikes. 

2. Increased flexibility

Because it acts so quickly, ultra-rapid insulin can be taken right before or even just after a meal, offering more flexibility than traditional insulins which often require planning and pre-meal timing.

3. Enhanced convenience

For those with busy lifestyles, ultra-rapid insulin simplifies the management of blood glucose levels around meals, reducing the stress and complexity of diabetes care.

4. Potential for better overall control

By improving post-meal glucose control, ultra-rapid insulin can contribute to better overall diabetes management, potentially reducing the risk of long-term complications associated with high blood glucose levels.

Considerations and usage

While ultra-rapid insulin offers significant benefits, it’s important to use it under the guidance of a healthcare provider. There may be some people for whom an ultra-rapid insulin may not be the drug of choice. For example, an elderly person or someone who suffers from severe hypoglycaemia may prefer an insulin that is absorbed more slowly.

Additionally, young children may be adversely affected if an ultra-rapid insulin is given prior to the meal and they do not complete the meal. However, due to its quick mode of action, an ultra-rapid insulin may be a good choice to give to a young child after the meal. It may also not be an option for those who make use of pump therapy.

As always, discuss the advantages and disadvantages with your doctor and ensure that it is the right fit for your diabetes management plan. Your doctor or diabetes educator can also provide the necessary instructions on proper dosing and timing to ensure optimal blood glucose control.

Final thoughts

Ultra-rapid insulin represents an exciting advancement in diabetes care, offering quicker action and greater flexibility. If you’re finding it challenging to manage your blood glucose levels around meals, or if you desire more freedom in your daily routine, talk to your healthcare provider about whether ultra-rapid insulin could be a suitable option for you. As with any medical treatment, individualised care and professional guidance are key to achieving the best outcomes.

Living with diabetes involves constant management and adaptation, but innovations like ultra-rapid insulin provide new tools to help make life easier and healthier. Embrace these advancements and work with your healthcare team to optimise your diabetes management plan. And always remember that there is no best insulin, or even best medication for diabetes. Each drug we use is as individual as the people themselves who live with diabetes. Know the options available and discuss with your healthcare provider which is the best fit for your lifestyle and individual needs.

Header image by FreePik

Dr Angela Murphy backs why metformin is still the drug of choice for treating Type 2 diabetes.

Listen to this article below or wherever you get your podcasts or visit our playlist.

Metformin was first described in the 1920s, but it was forgotten for years after the discovery of insulin. It was registered as a treatment for diabetes in the United Kingdom in 1958 and remains the most widely prescribed oral anti-diabetic medication.

Metformin is classified as a biguanide medication and was originally derived from the plant Galega officinalis, also known as French lilac.  It has several mechanisms of action which result in the lowering of blood glucose levels.

1. Decreases the production of glucose in the liver. It’s important to remember that the source of glucose in the blood is both from food and from the production of glucose in the liver.
2. Decreases the absorption of glucose from the gut.
3. Increases the uptake and utilisation of glucose by muscles. This is what improves insulin sensitivity.

Metformin doesn’t act on the pancreas to affect insulin production, so it’s unlikely to cause low blood glucose. Rather it helps to lower high glucose levels back to the normal range.

Figure 1: Hyperglucagonemia mitigates the effect of metformin on glucose production in prediabetes. (Konopka AR, et al. Cell Reports. 2016;15:1394.)

Metformin is registered in South Africa as a treatment for Type 2 diabetes. However, it can be used ‘off-label’ for other conditions, namely:

• Prediabetes
• Type 1 diabetes
• Polycystic ovarian syndrome

Prediabetes

Prediabetes is defined as one or both of the following being present:

• Impaired fasting glucose – This is a glucose level from 6.1mmol/L to 6.9mmol/L on a fasting blood sample.
• Impaired glucose tolerance – This is a glucose level from 7.8mmol/L to 11.1mmol/L on a blood sample taken two hours after a 75g glucose drink.

Metformin is often considered a reasonable treatment to introduce for prediabetes when attempts to normalise blood glucose with lifestyle interventions over a three to six-month period haven’t worked.

A strong family history of Type 2 diabetes (parents and siblings) would also increase the likelihood of metformin being offered in the setting of prediabetes.

Evidence from two large studies, the US Diabetes Prevention Program (DPP) and the Diabetes Prevention Program Outcome Study (DPPOS), has shown that metformin can prevent the onset of Type 2 diabetes in patients at risk. However, lifestyle intervention did give better results and should be encouraged first.

Type 1 diabetes

Type 1 diabetes is an autoimmune disorder that results in absolute insulin deficiency. This implies that, at diagnosis, the person with diabetes (PWD) must be given insulin injections. However, it’s possible for people with Type 1 diabetes to also be insulin resistant, particularly in the presence of obesity, sedentary lifestyle, and puberty.

The actions of metformin as described above, improving both liver and muscle insulin resistance as well as decreasing the absorption of glucose from the intestine, can improve the efficacy of insulin being injected in the person living with Type 1 diabetes. This would translate into lower insulin doses being required while glucose control improves.

One study found that people with Type 1 diabetes given metformin in addition to insulin showed better glucose concentrations, reduced insulin dose requirements, and some weight loss (on average 0.5kg).

Polycystic ovarian syndrome

Polycystic ovarian syndrome (PCOS) is diagnosed in women of reproductive age who have two of the following three criteria:

• Irregular menstrual cycles indicating irregular ovulation.
• Features of high male hormone levels: excess hair growth on face and body (hirsutism), acne, and baldness.
• An ultrasound scan showing polycystic ovaries.

An estimated 88% of women with PCOS are overweight or obese and almost three quarters have insulin resistance. Metformin has direct effects on the function of both the ovaries and the pituitary gland; the latter controls hormone functions in the body. This leads to improved menstrual cycles and fertility.

Metformin has been shown to induce ovulation either alone or with other hormonal drugs. Studies have suggested that metformin is more effective in women with PCOS who are also either overweight or obese. However, there are no specific predictors to show which women will respond better to metformin treatment.

The International Evidence-based Guideline for the Assessment and Management of Polycystic Ovarian Syndrome 2023 guideline states:

1. Metformin alone should be considered in adults with PCOS and a BMI ≥ 25 kg/m2.
2. Metformin alone could be considered in adolescents at risk of or with PCOS for cycle regulation, acknowledging limited evidence.
3. Metformin alone may be considered in adults with PCOS and BMI < 25 kg/m2, acknowledging limited evidence.

Figure 2: Clinical picture of polycystic ovarian syndrome (Rocha AL, Oliveira FR, Azevedo RC, Silva VA, Peres TM, Candido AL, Gomes KB, Reis FM. Recent advances in the understanding and management of polycystic ovary syndrome. F1000Res. 2019 Apr 26;8:F1000 Faculty Rev-565. doi: 10.12688/f1000research.15318.1. PMID: 31069057; PMCID: PMC6489978.)

Metformin side effects

Gastrointestinal: Diarrhoea, nausea, vomiting, abdominal pain, and flatulence. In these instances, the extended-release formulation of metformin can be tried (metformin XR). Especially taken at night, this is found to be better tolerated. If any of these gastrointestinal symptoms continue then metformin should be stopped, and another diabetic medication used.

Vitamin B12 deficiency: It’s important for patients using metformin over many years to have their vitamin B12 levels checked as metformin reduces the uptake of vitamin B12.

Low vitamin B12 causes neuropathy and particularly balance problems. This might be blamed on the diabetes whereas a more reversible cause could be present.

Kidney function: If a PWD’s kidney function drops too low, metformin dose will be reduced or even discontinued.

Lactic acidosis: A rare side effect of metformin when lactic acid builds up in the bloodstream, which usually only occurs when metformin continues to be given to critically ill patients.

Less common side effects include a loss of appetite and a metallic taste.

Figure 3: Metformin side effects. (Metformin and the Liver: Unlocking the Full Therapeutic Potential – Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/Most-common-side-effects-and-contraindications-of-metformin-and-metformin-associated_fig2_379291357 [accessed 14 Jul, 2024])

Facts and myths

In recent months there have been queries from PWD regarding the safety and benefit of metformin. There was obvious concern with the reporting of the presence of N-nitrosodimethylamine (NDMA) in metformin manufactured in the USA. Our own regulatory authority has been checking metformin in South Africa and to date no contamination has been found here.

The second wave of doubt arose, in my opinion, from an advertising campaign driving to sell supplements to treat diabetes. To create this market, they denounced the benefits of metformin.

Metformin has, in recent years, shown promise in augmenting the treatment of cardiovascular disease and stroke, cancer, Alzheimer’s and other dementias. It has anti-aging effects which may lead to longevity. None of these conditions are primary indications to use metformin, but for PWD taking metformin, they may derive extra benefits. We know for sure that less cancer is seen in people living with Type 2 diabetes taking metformin than in people living with Type 2 diabetes not taking metformin.

Metformin is still marvellous

In global diabetes management guidelines, including South Africa, metformin remains the first-line medication for the treatment of Type 2 diabetes.

Many new medications with multiple benefits to heart, brain and kidneys have been launched in the last two decades, but they have not dislodged metformin from its first-line spot.

Metformin remains an important treatment for Type 2 diabetes, has some accepted off-label indications and there is ongoing research to look at possible other clinical benefits.

References

1. Beysel S, Unsal IO, Kizilgul M, Caliskan M, Ucan B, Cakal E. The effects of metformin in type 1 diabetes mellitus. BMC Endocr Disord. 2018 Jan 16;18(1):1. doi: 10.1186/s12902-017-0228-9. PMID: 29338714; PMCID: PMC5771191.
2. org.uk 21 February 2023
3. Lashen H. Role of metformin in the management of polycystic ovary syndrome. Ther Adv Endocrinol Metab. 2010 Jun;1(3):117-28. doi: 10.1177/2042018810380215. PMID: 23148156; PMCID: PMC3475283.
4. https://www.monash.edu/__data/assets/pdf_file/0003/3379521/Evidence-Based-Guidelines-2023.pdf
5. https://www.health.harvard.edu/blog/is-metformin-a-wonder-drug-202109222605

Header image by FreePik

Dr Louise Johnson helps us understand how the big M (menopause) may affect the management of diabetes.

Listen to this article below or wherever you get your podcasts or visit our playlist.

Menopause is a normal condition involving the permanent end of the menstrual cycles due to the cessation of the production hormones from the ovaries for at least 12 consecutive months.

The name menopause comes from the Greek word pausis which means pause, and men which means month. Menopause occurs in all menstruating females due to oestrogen deficiency, usually between the ages of 45 and 56 in most women. The median age of natural menopause is 51 years.

As women live longer, they spend roughly 40% of their lives in the post-menopausal years which equates to more than 30 years for most women.¹

About 5% of women experience early natural menopause, occurring between the ages of 40 and 45 years.

Symptoms related to oestrogen deficiency

1. Vasomotor symptoms

These are the most common symptoms during menopause. Up to 80% of women experience vasomotor symptoms consisting of night sweat, palpitations, migraine, and hot flushes.

Hot flushes occur day and night at unpredictable intervals, often lasting approximately three to four minutes each. A hot flash starts with a sensation of flushing that spreads to the upper body due to the central nervous system changes specific to thermoregulation.

The vasomotor symptoms last on average one to six years but can last 15 years in 10 to 15% of post-menopausal women. They may be worsened by smoking, alcohol, obesity, physical inactivity, and emotional stress. If untreated, vasomotor symptoms will eventually dissipate after approximately 7.4 years.

2. Genitourinary symptoms

Approximately 50 – 75% of women experience genitourinary syndrome. The vagina lining thins and there is reduced elasticity. It causes vagina dryness, burning, pruritus (itchiness,) and irritation.

Urinary symptoms of frequently passing urine and the urge to go immediately occurs as well as burning urination. The low oestrogen levels in the bladder also cause frequent urinary tract infection.

Urinary incontinence is not related to menopause. The causes are overweight, diabetes, and increasing age. A decline in sexual function and libido is also part of the syndrome.³

3. Psychogenic symptoms

Up to 70% of women experience psychogenic symptoms associated with peri-menopause and menopause. These symptoms include anger, irritability, anxiety, tension, depression, loss of concentration, and loss of self-esteem and confidence.

Sleep apnoea, insomnia, and restless leg syndrome may cause further sleep disturbance that aren’t explained by night sweats. The risk of depressive symptoms and a higher level of depression severity are noted in the peri-menopausal women compared to pre-menopausal women.

Making a diagnosis

Physical examination

The following abnormalities are observed:

• Blood pressure is elevated.
• Weight gain is noted and an additional decrease in height associated with osteoporosis.
• Breasts have an increase in fatty deposition.
• Vagina has increase dryness and atrophy (wasting) of urethra (bladder pipe opening).
• Arthralgias (joint pains) and sarcopenia (loss of muscle mass, function and strength).

Lab tests

Tests are typically not needed to diagnose menopause. Under certain circumstances the following tests can be done:

• Follicle-stimulating hormone (FSH) will be increased. An elevated serum FSH greater than 30mIU/ml is an objective indicator of menopause.
• Oestrogen will be decreased. An oestrogen value less than 20pg/ml is suggestive of menopause.
• Thyroid stimulating hormone (TSH) to rule out an underactive thyroid since it can cause similar symptoms to those of menopause.

Staging

In 2011, The Stage of Reproductive Aging Workshop (STRAW) divided the female reproductive cycle into three categories:

1. Reproductive stage

This start with the beginning of menstruation. During these years the menstrual cycle is regular.

2. Menopausal transition stage

This is when peri-menopause occurs. During this stage, the menstrual cycle undergoes variability in duration of menstruation. As this stage progresses, women can experience no menstruation (amenorrhea) for a time of up to 60 days.

3. Post-menopausal stage

This stage begins when menstruation has ceased for up to one year.

Menopause and Type 2 diabetes

These are both conditions that often occur in midlife. Menopause causes a sharp drop in oestrogen levels, leading to various changes that can affect body weight, fat distribution, and insulin sensitivity. These changes can raise the risk for Type 2 diabetes or make managing your diabetes more challenging.

Menopause may increase the risk of developing Type 2 diabetes due to:

• Hormonal changes – Oestrogen and progesterone affect how cells respond to the hormone insulin. When oestrogen and progesterone levels drop, cells may not be as sensitive to insulin. This can lead to high glucose levels.
• Blood glucose fluctuations – Hormonal changes can cause blood glucose to fluctuate throughout the day. This can make managing diabetes a challenge.
• Weight gain – Menopause is commonly associated with weight gain, up to 7.5 kg. Excess weight is a known risk factor for Type 2 diabetes.
• Disturbed sleep – Menopause can lead to restless sleep due to night sweats and palpitations. A lack of sleep has been linked with a higher risk of Type 2 diabetes.
• Depression – Depression is more common in menopause than before it. People who are depressed may have an increased risk of diabetes due to increase eating and less exercise.²

Treatment

Menopause requires no medical treatment. Instead, treatment focus on relieving signs and symptoms and managing chronic conditions that may occur with aging. Treatments may include:

• Hormone therapy

Oestrogen therapy is the most effective therapy for relieving menopausal hot flashes. Your doctor may recommend the lowest dose for the shortest time frame to provide symptomatic relief. If you still have a uterus, you will require progesterone as well to prevent endometrium increase. Oestrogen helps bone loss, but the long-term use should be carefully considered due to the risk of breast cancer and blood clotting, such as deep venous thrombosis and pulmonary emboli (blood clot to the lung).

• Vaginal oestrogen

Oestrogen can be delivered directly to the vagina to prevent dryness, discomfort with intercourse, and some urinary symptoms. This modality is a lot safer than oral oestrogen and has a lot less complications.

• Low-dose antidepressant

Certain antidepressants related to the class SSRI, such as paroxetine, escitalopram or venlafaxine, may decrease hot flashes and help with depression and mood stabilising.

• Gabapentin

This drug is approved for seizures but has shown to reduce hot flashes.

• Clonidine

This tablet is typically used in high blood pressure but has shown to relieve hot flushes.

Lifestyle remedies

1. Drink enough cold water and dress in layers. Try to pinpoint your trigger that may include alcohol, caffeine, stress, and spicy food.
2. Decrease vaginal discomfort with a vaginal lubricant.
3. Get enough sleep by avoiding caffeine and too much alcohol.
4. Strengthen your pelvic floor by doing Kegel exercises.
5. Adopt a balanced diet.
6. Don’t smoke.
7. Exercise regularly. Do aerobic exercises, such as walking 30 minutes per day five days a week and weight-bearing exercises twice a week.

Remember that hormonal therapy comes with risks such as stroke, heart attacks, blood clots, and breast- and uterus cancer. Discuss with your healthcare provider and choose the correct treatment specific for you. Menopause is a condition that can be effectively managed by your health team.

References

1. Mangiome CM, Barry MJ et. al. “Hormone therapy for the primary prevention of chronic conditions in postmenopausal persons” JAMA 2022;328 (17):1740-46
2. Slopien R, Wender-Ozegowska E et. al. “Menopause and diabetes” Maturitas, 2018;117:6-10
3. Talauliker V.”Menopause transition:Physiology and symptoms” Best Praxct Res Clin Obstet Gynaecol. 2022,81:3-7

Header image by FreePik