Abstract
This article explores the intricate relationship between low-carbohydrate diets, particularly very low-calorie ketogenic diets (VLCKD), and hypothyroidism, considering their effects on thyroid hormone levels and overall thyroid function. We will examine the potential benefits and risks associated with these diets for individuals with or at risk of developing hypothyroidism.
Introduction to Very Low-Calorie Ketogenic Diets (VLCKDs)
Very low-calorie ketogenic diets (VLCKDs) are dietary interventions characterized by a high proportion of calories derived from fat (around 90%) and a smaller proportion from carbohydrates and proteins (approximately 10%). These diets have gained popularity not only for weight loss but also for potentially reducing the severity of various obesity-related disease states. The Italian Society of Endocrinology (SIE) has endorsed VLCKD for managing several obesity-related conditions, including hypertension, dyslipidemia, and type 2 diabetes mellitus. The European Association for the Study of Obesity (EASO) also recommends VLCKD as a personalized nutritional treatment option for patients with obesity.
VLCKDs involve a significant reduction in carbohydrate intake while increasing the proportion of calories from fat and protein. These diets have been shown to exert a beneficial influence on metabolic parameters, such as blood pressure, glycemia, and lipid levels, in addition to promoting weight loss. In the management of epilepsy resistant to standard treatments, KD has been employed, with the belief that switching from glucose to ketone body metabolism positively affects the regulation of certain neurotransmitters, oxidative stress, and ion channels. Current evidence suggests that the effectiveness of KD extends to various pathologies, including impaired glucose control, obesity, polycystic ovary syndrome, cancer, and psoriasis. KD has also been studied as a tool to preserve muscle mass in the context of weight loss programs.
Animal studies have demonstrated that VLCKD inhibits cortisol production, influencing metabolic and endocrine regulation. Additionally, VLCKD can decrease renin while increasing aldosterone levels in patients with obesity, thereby reducing blood pressure.
Understanding Hypothyroidism
Hypothyroidism, characterized by an underactive thyroid gland, affects a notable percentage of the general population, with prevalence ranging from 0.3% to 7%. This condition can arise from various factors, including autoimmune disorders, congenital conditions, pregnancy, certain medications, irradiation, thyroidectomy, and iodine deficiency. Hypothyroidism can lead to significant health consequences, including myxoedema coma and an increased risk of heart failure and stroke in younger individuals, and has also been linked to cognitive problems.
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Dietary choices, weight loss, and changes in body mass index (BMI) can impact thyroid hormone levels. Individuals with obesity have a higher prevalence of subclinical hypothyroidism (sHypo) compared to those without obesity. In patients with obesity, identifying and managing sHypo can present challenges. Individuals with euthyroid obesity exhibit higher thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), and fT3/fT4 ratios compared to patients without obesity with the same condition. Studies in both animals and humans have reported an association between diet and T3, thyroxine (T4), and TSH levels, with a high-fat and low-carbohydrate caloric distribution shown to affect the thyroid profile.
VLCKD Protocol: A Step-by-Step Approach
The VLCKD protocol involves three key steps: active, re-education, and maintenance, which must be discussed with the patient. It's crucial to highlight the strict contraindications associated with VLCKD before starting the protocol. These contraindications include moderate renal failure, type 1 diabetes mellitus, latent autoimmune diabetes in adults, sodium/glucose cotransporter 2 inhibitor use, and cell failure in type 2 diabetes. Additionally, chronic to severe kidney disease, liver failure, heart failure (NYHA III-IV), unstable angina caused by respiratory failure, recent myocardial infarction or stroke (within the past 12 months), cardiac arrhythmias, and eating disorders are among the conditions where this diet is not recommended.
The first 8-12 weeks involve reduced carbohydrate intake to induce nutritional ketosis. During the initial stage, the diet consists of very few calories (650-800 kcal/day) and is low in carbohydrates (less than 30 g daily from vegetables) and fat (only 20 g per day, derived from olive oil). The protein intake of high-biological-value ranges between 1.2 and 1.4 g per kilogram of ideal body weight, intending to preserve lean body mass. Protein can be obtained from common foods like eggs, meat, or fish, or can use meal replacements instead. Current scientific evidence supports the use of meal replacements during the first active ketogenic phase, ensuring safe, effective, and controlled administration of VLCKD. Tailored meal replacement options offer a more precise calibration of an individual's dietary intake, enabling precise and personalized adjustment of the calorie, macronutrient, and micronutrient content required by the patient.
Following the initial active ketogenic phase, a LCD is advised, during which time other food categories are gradually resumed. In particular, foods with the lowest glycemic index-like fruits and dairy-are the first to be progressively reintroduced, along with carbohydrates. The LCD diet calls for a daily caloric intake of 1000 - 1200 kcal, along with 60 - 100 g of carbohydrates. After that, a hypocaloric balanced diet is maintained, reintroducing legumes and consuming 1300 - 1400 kcal and 130 - 150 g of carbohydrates.
It is essential to maintain a hypocaloric balanced diet that follows the Mediterranean diet with a caloric intake between 1500-2200 kcal in the final maintenance stage. This diet should include low glycemic index cereals. Adopting healthy eating habits is vital for sustaining long-term results effectively. According to research, it is critical for patients with obesity to reduce body weight by at least 15% and maintain that reduced weight in order to decrease their cardiometabolic risk per kg of desirable weight (i.e., weight corresponding to a BMI of 22.5 kg/m2). High-fiber foods with slow-absorbing starches are recommended sources of carbohydrates; excessive simple sugar intake (max 10%) should be avoided, and instead, opt for a diet that is abundant in cereals, fruits, vegetables, and legumes. Patients can use this dietary pattern to maintain weight loss while remaining in their nutritional re-education.
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The Interplay Between Hypothyroidism and Obesity
The connection between obesity and hypothyroidism is a subject of continuous discussion in the medical community, particularly relevant given the increasing rates of global obesity. While patients often perceive obesity as a consequence of thyroid malfunction, it remains unclear whether subclinical hypothyroidism (sHypo), as opposed to overt hypothyroidism, is associated with weight gain. Thyroid dysfunction can cause changes in weight, temperature, and energy expenditure, regardless of physical activity. Hypothyroidism is related to a decrease in the body's ability to produce heat, a reduction in metabolic rate, and an increase in BMI and obesity.
Some experts suggest that changes in TSH levels may be a consequence of obesity rather than the cause. Recent research has revealed a connection between obesity and thyroid autoimmunity, with the hormone leptin produced by adipose tissue as the primary link. Studies have shown that even small changes in levothyroxine (L-T4) dosage during replacement therapy can cause significant variations in resting energy expenditure in hypothyroid patients. There is insufficient data on the amount of weight gain or loss associated with L-T4 treatment for hypothyroidism.
An inverse relationship exists between fT4 and BMI, even when fT4 levels are within the normal range. In individuals who are slightly overweight but still have normal thyroid function, fat accumulation is linked to lower fT4 and higher TSH levels, resulting in an increase in body weight over time. This issue suggests that changes in energy expenditure due to altered thyroid function may be a primary factor leading to an increase in body weight, even with normal feedback regulation. Low fT4 levels and a moderate increase in T3 or fT3 levels are observed in individuals with obesity. Research shows that fat accumulation is related to increased TSH and fT3 levels, independently of insulin sensitivity and metabolic parameters. Furthermore, in patients with obesity, the fT3 to fT4 ratio is positively associated with BMI and waist circumference. Numerous research findings supported the notion that patients with obesity had higher levels of circulating TSH and fT3 than subjects with normal weights. Interestingly, TSH and fT3 changes were completely reversible following significant weight loss (33% BMI decrease). These findings underscore the pivotal role of adipocytes in the regulation of TSH and thyroid hormones, suggesting that obesity can cause peripheral and central thyroid hormone resistance.
Low-Carb Diets and Thyroid Hormone Conversion
Low-carb and ketogenic diets have become popular for weight loss, at least in otherwise healthy individuals. The standard Western diet consists of about 50-60% energy from carbohydrates, or roughly 300 grams per day. Low-carb diets restrict carbohydrates to less than 30% of total energy intake, while ketogenic diets restrict them to less than 10%. This restriction forces the body to switch to ketones for energy, which are produced from fats, rather than glucose from carbohydrates.
Carbohydrate intake appears to influence the amount of T3 that gets converted from the T4 thyroid hormone. Glucose and thyroid hormones rely on each other synergistically. Studies suggest that severe calorie restriction can limit the conversion of T3 from T4, which is undesirable for hypothyroidism. A very low-carb ketogenic diet may have a similar effect because of the way it mimics starvation or fasting metabolically.
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Research Findings on Ketogenic Diets and Thyroid Function
A randomized crossover-controlled study involving eleven healthy, normal-weight participants investigated the effects of a ketogenic diet (KD) and a high-carbohydrate, low-fat (HCLF) diet on thyroid function. For a minimum of three weeks on each, participants followed two isocaloric diets: a HCLF diet (55%carbohydrate, 20%fat, 25%protein) and a KD (15%carbohydrate, 60%fat, 25% protein), with a one-week washout period in-between. Importantly, while on the KD, the participants were required to remain in a state of nutritional ketosis for three consecutive weeks. Both dietary interventions resulted in significant body mass loss however three weeks of sustained ketosis (KD) resulted in a greater loss of body mass than did three weeks on the HCLF diet. Compared to pre-diet levels, the change in plasma T3 concentration was significantly different between the two diets, such that plasma T3 concentration was significantly lower following the KD diet but not different following the HCLF diet. There was a significant increase in T4 concentration from pre-diet levels following the KD diet, but not following the HCLF diet. The magnitude of change in plasma T4 concentration was not different between the two diets. There was no effect of diet on plasma thyroid stimulating hormone concentration. Although the diets were isocaloric and physical activity and resting metabolic rate remained constant, the participants lost more mass after the KD than after the HCLF diet.
Higher levels of thyroxine (T4) with no change in triiodothyronine (T3) have been reported in one study, while in another, ketosis resulted in lower levels of T3. Several other studies have reported reductions in T3 with carbohydrate restriction, but there are limitations to these studies as the majority had small samples sizes and perhaps, more importantly, measurements in those studies were done after only four or seven days of carbohydrate restriction. The utilization of ketone-bodies (accounting for 50-85% of oxidative metabolism) becomes significant only after three to seven days of starvation Hence, in these latter studies, the participants may not have reached nutritional ketosis, and so would not have had time to become “keto-adapted”; a state in which a coordinated set of metabolic adaptations have occurred that ensure appropriate inter-organ fuel supply given the reduced availability of glucose.
Alternative Dietary Approaches for Hypothyroidism
If you’re living with hypothyroidism, a doctor will usually recommend anti-inflammatory eating plans, such as the Mediterranean diet. The keto diet is not typically recommended.
There isn’t a hypothyroidism diet per se, but certain eating styles may help support your overall thyroid health. One 2022 research review indicated that anti-inflammatory eating plans may have a positive effect on hypothyroidism. A few notable examples include the Mediterranean diet as well as different types of plant-based diets.
The Mediterranean diet is an eating pattern that consists mostly of vegetables, fruits, and whole grains, as well as healthy fats, legumes, and occasional meats. Due to its inherent antioxidant-rich foods, it’s also commonly prescribed for thyroid diseases like Hashimoto thyroiditis. Foods included in the Mediterranean diet are also natural sources of important micronutrients that can support thyroid health. These include: vitamin A, vitamin B12, vitamin D3, iron, selenium, and zinc.
Plant-based diets may also support hypothyroidism. These diets can still include meat, but meat is not the primary focus of your meals. According to one 2020 research review, people who follow vegan diets, for example, have less inflammation and are better able to maintain a moderate weight. The authors also noted that veganism may help prevent autoimmune thyroid diseases.
In terms of what to add to your diet, you may first consider some of the foods eaten as part of a Mediterranean or plant-based lifestyle. Examples include: fresh vegetables, fruits instead of sugary sweets, fish, chicken, and turkey, healthy fats, such as avocados and olive oil, whole grains, such as oats and brown rice, beans, nuts, and legumes.
People with hypothyroidism may need to be cautious with excess amounts of iodine. The mineral can be found in supplements, as well as certain seaweed and kelp. A doctor may also recommend that you limit: sugars, processed foods, caffeine, alcohol.
Practical Considerations for Managing Hypothyroidism with Diet
It’s important to talk with a doctor before trying any particular diet for hypothyroidism. Eating and avoiding certain foods may support your thyroid health, but you will still need ongoing treatment and regular blood tests to ensure your body is getting the appropriate amount of thyroid hormones.
For most people, according to the ATA, it’s best to take thyroid replacement medications in the morning before breakfast. This way, your body has a chance to absorb the hormones before food, supplements, and other medications may interfere with this process. The British Thyroid Foundation reports that for thyroid hormone replacements to be the most effective, you should take them at least 30 minutes before eating a meal. You’ll also want to avoid eating soy and grapefruit within a few hours of taking your medications, as these may decrease thyroxine (thyroid hormone) absorption.
Whether you’re wanting to change your eating pattern for weight management or for overall health, it’s important to not focus on restrictive diets that may promise quick results. The keto diet is one such plan that does not support hypothyroidism.
Low-Carb Diets: Impact on Thyroid Function
A low-carbohydrate diet, frequently used for treatment of reactive hypoglycemia, hypertriglyceridemia, and obesity may affect thyroid function. Carbohydrates are sugar (glucose), and we associate sugar with weight gain. After eating, your body breaks carbs down into individual sugar molecules. Your cells use this sugar as their primary energy source. Without an energy source, your cells have a hard time functioning. It’s like a car: without gas, it won’t work.
There are two main types of dietary carbs - simple and complex. A simple carbohydrate is a straight-up sugar. It is the sugar you put in your coffee or in regular soda and processed foods. But simple sugars are also found naturally in fruits, vegetables, and milk. Complex carbohydrates are .formed from many simple sugar molecules. This group is further broken down based on whether your body can digest them. Here are two examples of complex carbohydrates: Starches are broken down into simple sugars. Common starches include rice, potatoes, peas, and corn. Fiber can’t be broken down by your body. Foods with fiber leave you feeling full longer and can help prevent constipation and lower cholesterol and blood sugar levels. Fiber is found naturally in fruits, vegetables, nuts, seeds, beans, and whole grains.
Conventional nutritional guidance recommends that about 50% of your food be carbohydrates. The recommended Daily Value for carbohydrates, as seen on Nutrition Fact labels, is 275 grams daily. But, this amount varies based on age, health conditions, and weight status. Low-carb diets limit the amount of carbs you can eat, sometimes between 25 grams to 150 grams per day. Examples of low-carb diets include the ketogenic diet, low-carb paleo, and the Atkins diet.
Effects low-carb diets have on your thyroid:
- Thyroid hormones influence your metabolism or how your body uses energy. When your thyroid hormone levels are too high, your metabolism speeds up. Low thyroid hormone levels -- hypothyroidism -- causes your metabolism to slow down. The production of thyroid hormone depends on a constant energy source. Restricting carbohydrate intake can decrease your thyroid’s ability to produce and secrete thyroid hormone. Ultimately, this can leave you feeling more tired or sluggish.
- Your thyroid makes two types of thyroid hormone: the inactive T4 (thyroxine) and the active hormone, T3 (triiodothyronine). Most thyroid hormone secreted is T4, which needs to be converted into T3, the active form. This conversion requires a specific enzyme called 5’-deiodinase. Low-carb diets can reduce the activity of this enzyme, resulting in low levels of T3 production.
- Carbohydrates trigger the release of insulin, a hormone that regulates blood sugar levels by moving the sugar into your cells. Once inside, your cells use sugar for energy. If your body does not get enough carbs over time, this can impact how your cells respond to insulin, known as insulin sensitivity. A decrease in insulin sensitivity means your cells can’t move sugar into your cells, thus, impacting how they function. In the case of your thyroid, the outcome would be a lack of thyroid hormone production.
- Low-carb diets mimic a fasting state, causing your body to rely on other macronutrients for energy. Gluconeogenesis is the process of making sugar from a non-carbohydrate source. Gluconeogenesis increases slightly in those following a low-carb diet. But gluconeogenesis can’t make enough sugar to supply all your cells with a constant energy source. Evidence shows that during a state of fasting, your T3 levels decrease.
In summary, carbohydrates are an essential energy source for all your cells, including your thyroid cells. Not eating enough carbohydrates impacts thyroid hormone production, conversion, and regulation. Thus, low-carb diets may disrupt your thyroid function.
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