In 1988, Gerald Reaven delivered his seminal lecture on the Role of Insulin Resistance in Human Disease, where he defined insulin resistance as reduced sensitivity to insulin-stimulated glucose uptake and pronounced it a key feature of T2D, hypertension and coronary artery disease.²⁵ He recognised the cluster of features, which he named Syndrome X, now called metabolic syndrome, as downstream features of insulin resistance and identified glucose intolerance, elevated triglycerides, low high-density lipoprotein cholesterol (HDL-c) and hypertension to be associated with chronic disease (see Table 2).

Reaven understood that insulin resistance alone did not determine the degree of glucose intolerance but that the ability of the pancreatic β-cells to compensate for insulin resistance by increasing insulin secretion is crucial in maintaining normal glucose tolerance. Individuals with severe insulin resistance but robust β-cell compensation can remain normoglycaemic, while those who cannot sustain hyperinsulinaemia develop hyperglycaemia and eventually T2D. In T2D, there is resistance to insulin-stimulated glucose uptake as well as to insulin suppression of plasma free fatty acid (FFA) concentrations. Elevated FFAs can stimulate hepatic glucose production, contributing to fasting hyperglycaemia.

Reaven also noted insulin resistance was common in those with hypertension and that antihypertensive treatment did not address the metabolic abnormalities, positing insulin resistance, via its action on the sympathetic nervous system and enhanced renal sodium reabsorption, could be the mechanism driving hypertension.²⁵ Other consequences of insulin resistance include proliferation of vascular smooth muscle, increased sympathetic nervous system activity and diminished release of nitric oxide from the endothelium.^28,29

Numerous studies now support hyperinsulinaemia as an independent risk factor for CVD, with associated hypertriglyceridaemia and low HDL-c.^30,31 In addition, we now know there exists heterogeneity in insulin resistance and β-cell dysfunction between individuals and deficiencies in incretin action and hepatic glucose regulation also occur in patients who develop T2D. Metwally et al. recently identified four phenotypes of metabolic dysregulation.³² These may be loosely grouped as an insulin-resistant dominant subphenotype (muscle and liver insulin resistance – highly intercorrelated) and an insulin secretion subphenotype (β-cell function and incretin deficiency). These phenotypes may not correlate with standard measures of glucose regulation such as haemoglobin A1c (HbA1c).³²

Insulin resistance is a common feature of overweight and obesity, and academic discussion continues as to the precise mechanisms contributing to weight gain.^33,34

The carbohydrate-insulin model (CIM) of obesity posits that a high-carbohydrate diet (particularly rapidly digestible carbohydrates in the form of starchy foods and sugar) promotes homeostatic dysregulation, driven primarily by postprandial hyperinsulinaemia.³³ While weight gain can result from various mechanisms, insulin primarily drives anabolic pathways. It stimulates glucose uptake into tissues and inhibits the release of fatty acids from adipose tissue and ketone production, driving fat and glycogen storage.³³ In this model, overconsumption is a consequence of increasing adiposity rather than the driving factor of weight gain. The CIM acknowledges that the insulin response to carbohydrate varies with individuals and that influences individual responses to different diets, where those who exhibit an intrinsically higher insulin response to carbohydrates may be more vulnerable to weight gain on a higher (particularly high-glycaemic load) carbohydrate diet.³³ A key tenet of the CIM is that the metabolic effects of reducing carbohydrates in the diet drive weight loss via increasing the metabolic rate, and that this has a greater influence than reducing dietary fat or energy intake.^35,36 This has been demonstrated by observing an increase in energy expenditure during a reduced-carbohydrate weight loss maintenance period.³⁷ Reduced carbohydrate approaches specifically target insulin signalling, which is a key component of this model.

Others hypothesise that the brain is primarily responsible for excessive weight gain through external and internal signals in response to the food environment. They posit that various hormones impacting neuroregulatory pathways drive imbalances in food intake and fuel partitioning, promoting fat storage. This is also known as the energy balance model (EBM).³⁴

Reduced carbohydrate approaches also target neurobiology via various mechanisms, and over time, both hypotheses have expanded their definitions, and an integrated model was proposed by Ludwig and Sørensen in 2022.³⁸ The competing hypotheses agree that^33,34,39:

Macronutrient composition impacts hormonal signalling and thus influences satiety.⁴¹ Targeting adequate protein intake is a feature of TCR, and increasing protein in the diet has been associated with increased satiety when carbohydrate content has been kept stable.⁴² A study from Darcey et al. has shown that the metabolic and neurological effects of fat-restricted diets (low-fat) influence subsequent ad libitum food intake towards foods higher in carbohydrate and fat, suggesting macronutrient effects on brain-reward regions.⁴³ Reducing fat in the diet reduced dopamine tone in brain-reward regions, making adherence more challenging. This effect was not observed in the reduced-carbohydrate arm. They posit, ‘Results suggest that “a calorie is not a calorie,” when it comes to macronutrient effects on brain-reward regions in humans’.⁴³

In real-world settings, via various potential mechanisms, a reduction in energy intake usually occurs spontaneously with carbohydrate reduction.^44,45 Therefore, this, along with increased energy expenditure, may play a role in the weight loss commonly seen with TCR. Therapeutic carbohydrate reduction addresses the core features implicated in obesity and other metabolic disorders, as discussed in ‘Mechanisms of action of therapeutic carbohydrate reduction for metabolic disorders’ section.

As fibre constitutes the main carbohydrate component of a whole-food TCR approach, a total carbohydrate approach ensures the most consistent results. Net carbohydrate counting (total carbohydrate minus fibre and/or sugar alcohols) could theoretically be applied to fruit and vegetables, as fibre is not typically metabolised to glucose; however, assessing patient responses to total carbohydrate intake and adjusting upwards if tolerated appears to be the most straightforward approach. Fibre intake may be adjusted according to patient responses and therapeutic goals. While general TCR provides adequate fibre and has been shown to favourably influence the gut microbiome,⁹⁷ diets lower in fibre in the context of TCR may be considered because of the adaptability of the gut microbiome and ketone metabolites.^98,99 Emerging evidence has demonstrated that a zero-carbohydrate exclusion protocol (no fibre) may have benefits for select cases of gastrointestinal disorders and suggests fibre is not essential for bowel health.⁵¹ An individualised approach that accounts for patient physiology and preferences is recommended. For example, a low-fibre diet may benefit cases of chronic constipation.¹⁰⁰

Adequate dietary protein may be achieved with a range of dietary patterns. Animal-sourced foods contain the full complement of amino acids (20) and all nine essential amino acids (EAAs). Plant proteins are combined with the plant fibre matrix, reducing bioavailability,¹⁰¹ which may need to be accounted for when using whole-food plant protein sources, as plant-based protein powders are typically stripped of their fibre content. Vegetarian or vegan carb-restricted dietary patterns should be well formulated to meet protein requirements. It may be necessary to consider the higher carbohydrate content of protein sources, and supplementation should be considered if needed. Vulnerable patients (e.g. those with sarcopenia or cachexia) may benefit from more precise protein goals. An estimated intake of at least 25 g – 30 g of high-quality protein per meal is suggested for maximum stimulus of muscle synthesis across all ages.^46,94

A well-formulated carbohydrate-reduced diet includes full-fat dairy and other whole foods containing a variety of fatty acids (i.e. unprocessed meats, avocados and olives), which are not typically restricted.

Saturated fats, containing different types of saturated fatty acids (SFA), are required for a range of key biological functions and are required for the absorption of fat-soluble vitamins (A, D, E and K). Despite concern in recent decades, current evidence builds on previous analyses, which do not support the restriction of saturated fat for CVD prevention.^102,103,104

Industrial trans fats, produced by the partial hydrogenation of vegetable oils, should be avoided because of their adverse impact on metabolic health via inflammation, endoplasmic reticulum stress and lipid metabolism.^105,106 Many countries have banned or capped the use of trans fats, and these fats are generally contained in processed foods, which are not recommended in TCR. Naturally occurring trans fats are produced in the stomachs of ruminant animals and found in dairy and meat. These subtypes do not demonstrate harmful effects at levels typically consumed (trace amounts) and appear neutral or even mildly beneficial.^107,108

A complicating comorbidity because of historical data and differences with emerging TCR data is chronic kidney disease (CKD). Historically, there have been concerns about protein consumption in the context of low-carbohydrate diets and the potential for harm in patients with CKD.¹¹⁸ However, a recent Cochrane review compared low protein (0.6 g/kg/day – 0.8 g/kg/day) with unrestricted (≥ 1.0 g/kg/day) protein for at least 12 months and found uncertainty regarding the benefits of protein restriction.¹¹⁹

Practically, target protein levels for reduced carbohydrate diets often fall between 1.2 and 1.5 g/kg body weight, which is comparable to average protein intakes when consuming a standard American diet (at approximately 15% – 20% of daily energy expenditure) and can be below the ‘high protein’ threshold thought to be between 1.5 and 2.0 g/kg.^46,89,120

In patients with kidney disease, there is uncertainty about optimal levels of protein intake, especially where nutritional sufficiency is compromised.¹²¹ A meta-analysis from 2018 examining the effect of protein restriction on CKD progression concluded:

A prudent approach in individuals with CKD is to aim for 0.8 grams of protein per kg per day, which is feasible with TCR and aligns with a clinical practice guideline (KDIGO 2024).¹²² The guideline suggests avoiding high protein intake (> 1.3 g/kg body weight/d) in adults with CKD at risk of progression. They make allowance for clinical judgement in cases of frailty and sarcopenia where higher protein targets may be considered, and protein restriction is not recommended in children with CKD.¹²²

Table 10 summarises data on several studies using various forms of therapeutic carbohydrate reduction in patients with mixed grades of CKD (see Table 10).

Tirosh et al. conducted a 2-year randomised controlled trial in individuals with obesity, with or without T2D, comparing low-carbohydrate (20 g/day for 2 months, increasing gradually up to a maximum of 120 g/day), Mediterranean and low-fat diets. They found that a low-carbohydrate diet did not adversely affect renal function, as measured by estimated glomerular filtration rate (eGFR) and urinary microalbumin-to-creatinine ratio, in moderately obese participants with or without T2D.¹²³ Friedman et al. conducted a secondary analysis of a long-term trial that compared a low-carbohydrate diet (20 g/day for 12 weeks, followed by a gradual increase in carbohydrate intake to maintain weight stability) with low-fat diets in obese adults. The study found no significant harmful effects on renal filtration indices, including serum creatinine, cystatin C and creatinine clearance, over a 2-year period.¹²⁴ Tay et al. conducted a randomised trial comparing a very low carbohydrate, high-protein (14% energy as carbohydrate [CHO < 50 g/day], 28% protein [PRO], 58% fat [< 10% saturated fat]) diet to a high-carbohydrate diet (53% CHO, 17% PRO, 30% fat [< 10% saturated fat]) in individuals with T2D.¹²⁵ The study found no decrement or difference between groups on clinical markers of renal function, such as eGFR and albumin excretion rate, over 12 months.

Recent evidence has shown TCR to be safe for patients with mild CKD, and a number of studies suggest TCR may result in improved kidney function.^{89,127,128,129} In a recent study of adults with T2D, a ketogenic diet (initial CHO < 30 g/day, protein target 1.5 g/kg of reference body weight) was linked to improved (from stage 3 to stage 2 or stage 4 to stage 3) or stable kidney function and reduced inflammation over 2 years, with greater benefits observed in those achieving higher levels of sustained ketosis.⁹⁰ A small study using a very low carbohydrate diet (CHO ≤ 30 g/day, protein not specified) has demonstrated improvements in metabolic health with reduced medication burden in patients with grade 3–4 kidney disease and stabilised renal function (15/18 participants improved eGFR score).¹²⁶ Further studies are needed in the setting of advanced CKD, but there is growing evidence that TCR may be beneficial in those with CKD whose renal function is less compromised.

For autosomal-dominant polycystic kidney disease (ADPKD), a ketogenic diet has been shown to be feasible^130,131 and has demonstrated early, promising results, with the potential to improve kidney function.^132,133 Cukoski et al. recommended 0.8 g of protein/kg of body weight per day, and maximum carbohydrate intake was set at 30 g.¹³¹

There is an emerging body of evidence supporting the use of TCR for MASLD, previously referred to as non-alcoholic fatty liver disease (NAFLD). This term acknowledges metabolic dysfunction as a driving cause of the disease and describes a range of liver diseases from hepatic steatosis to steatohepatitis (inflammatory), which may lead to fibrosis and cirrhosis.⁷⁷ Watanabe et al. reviewed evidence and concluded a ketogenic diet to be safe and therapeutic for MASLD (framed as NASH in the review) and suggested it could be considered until end-stage liver disease under the evaluation and care of a skilled hepatologist.^110,134 A very low-calorie ketogenic diet was initiated for two patients with end-stage liver disease to help them meet eligibility for a liver transplant. Both patients lost weight without adverse effects.¹³⁴ A number of studies have shown the benefit of TCR for MASLD,⁷⁷ with some evidence that more severe steatosis demonstrates a greater treatment response compared to milder disease.¹³⁵

Though more research is needed, overall, TCR has demonstrated a benefit for MASLD, which should be considered on a case-by-case basis by an experienced clinician with appropriate monitoring.

There is limited data on the safety of prolonged ketosis for foetal development; glucose availability is essential for growth. Healthy pregnant women undergo metabolic fluctuations throughout pregnancy to support foetal growth and development. Studies show that pregnant women appear to enter ketosis more readily, and this is accentuated in the third trimester.¹³⁶ This may contribute to the rare cases of ketoacidosis occurring in pregnancy, usually provoked by concurrent illness.⁶² This susceptibility extends to lactation, where cases of lactation ketoacidosis have occurred.¹³⁷ In addition, pregnant women with abnormal glucose metabolism are more likely to enter ketosis.

Various guidelines acknowledge pregnancy is a ketogenic state, and the emphasis is on avoiding ketoacidosis in the context of gestational diabetes mellitus (GDM).^138,139 Monitoring ketones is suggested by some bodies.¹³⁸ There is a lack of studies specifically addressing mild ketosis during pregnancy. However, it is known that ketone bodies diffuse across the placenta and the placenta contains enzymes capable of converting acetyl-CoA into beta-hydroxybutyrate.¹³⁶ There is some evidence that ketones provide energy for the foetal brain, possibly contributing to brain development, though overall it is difficult to draw conclusions about the effect of elevated ketone levels on the fetus.¹³⁶ Healthy neonates are often in ketosis.¹⁴⁰ A review by Tanner et al. states:

If clinically indicated (e.g. diabetes or other conditions being managed by TCR), measuring ketones in this situation could offer a way to safely manage carbohydrate reduction in pregnancy and avoid ketonuria. The American Diabetes Association (ADA) suggests ketones can be measured to identify patients who are ‘severely restricting carbohydrates to manage blood glucose’.¹⁴¹ Including starchy vegetables or low-glycaemic index (GI) fruit in the diet to prevent ketosis is one approach to consider (ensure carbohydrate intake exceeds 50 g/day). The ADA also states that a ‘food plan should provide adequate calorie intake to promote foetal/neonatal and maternal health, achieve glycemic goals and promote appropriate weight gain’,¹⁴¹ which may be achieved using a variety of nutritional approaches. An excellent resource for women and clinicians may be found in Real Food for Pregnancy by Lily Nichols.¹⁴²

Historically, gestational diabetes was managed successfully using reduced carbohydrate approaches (30% – 40% of total calories from carbohydrate), where the goal was to avoid ketonuria but prevent postprandial hyperglycaemia.^143,144 Jovanovic-Peterson et al. studied women with insulin-dependent diabetes with the aim of achieving euglycaemia but avoiding ketonuria.¹⁴⁴ Carbohydrate intake was adjusted to 30% – 40% TEI to keep 1-h postprandial blood glucose < 140 mg/dL (7.8 mmol/L) and avoid ketosis. For example, a 60 kg woman (deemed to be in the ‘normal weight’ range, assigned 30 kcal/kg) would be given 90 g of protein (~1.5 g/kg or 20% TEI) with 30% carbohydrate, estimated at 135 g/day, depending on biofeedback. Their data on 52 women using this approach (with documented euglycaemia) found the rate of complications in the control group (non-diabetic) exceeded that of the intervention group (with insulin-dependent diabetes).¹⁴⁵

More recently, a low GI diet (carbohydrate-reduced diets sit at the lower end of the low GI spectrum) has been associated with less frequent insulin use and less macrosomia than control diets.¹⁴⁶ Ásbjörnsdóttir et al. found that ‘lower daily carbohydrate consumption than recommended by the Institute of Medicine is common among women with T2D in early pregnancy in Denmark’.¹⁴⁷ A small percentage of the women with type 1 and T2D reported consuming less than 100 g of carbohydrates daily (mean 83 and 78 g, respectively), with no ketonuria reported at the first antenatal visit.¹⁴⁷ Mijatovic et al. randomised pregnant women to a moderately carbohydrate-reduced diet (~135 g/d carbohydrate) or routine care (~200 g/d), looking at blood ketone concentration, risk of ketonaemia and pregnancy outcomes. While difficulties with adherence prevented definitive conclusions, these data suggest a modest reduction of carbohydrates is feasible without ketonuria, which may be monitored.¹⁴⁸ An excellent resource for women and clinicians may be found in Real Food for Gestational Diabetes by Lily Nichols.¹⁴⁹

Breastfeeding can increase the risk of lactation ketoacidosis, a rare but serious condition. If TCR is clinically indicated, consider avoiding ketonuria by incorporating starchy vegetables or fruit (> 50 g carbohydrate/day) and monitoring ketone levels. The literature reports the composition of the breast milk may be higher in protein content but otherwise unremarkable.¹⁵⁰ If medically indicated (e.g. mother or infant with epilepsy), reduced carbohydrate approaches may be successful with appropriate monitoring and medical supervision.¹⁵¹

Both gout and gallbladder disease are strongly associated with insulin resistance, and, overall, TCR may be expected to benefit these conditions.

In gallbladder disease, it is thought that low HDL-c and high triglycerides increase the cholesterol saturation index, promoting the development of cholesterol crystals, which are a precursor to gallstone formation. Diets higher in fat have been shown to be protective for the development of gallstones during periods of weight loss,¹⁵² and TCR improves triglyceride and HDL-c markers.¹⁵³ A more gradual transition to increased fat in the diet is advised, especially where a cholecystectomy has been performed.¹⁵⁴

Patients with a history of gout are at a higher risk of flare when transitioning to the diet, although long-term gout flares may improve on low-carb diets.¹¹⁵ Short-term increases in uric acid concentration may occur as ketone bodies and uric acid compete for the same excretion pathways. This resolves over 2–8 weeks, but consistent adherence may be preferable in this setting.⁸⁹ Consider prophylaxis during transition.

Clinical tests:

Blood tests:

Urine tests:

Consider these additional tests depending on the clinical circumstances:

Maintaining hydration and sodium intake are key during adaptation, as this manages many of the symptoms. For most patients, 2 g – 3 g of sodium (or 5 g – 7 g of salt) per day is appropriate. This can be accomplished by salting food liberally or adding salt to bone broth.⁴⁶ The dose may be adjusted over time as per individual requirements. Proprietary brand electrolyte solutions may also be useful.

Potassium may also become depleted in the setting of inadequate sodium intake and can present as muscle twitches or weakness, cramps or irregular heartbeats (and constipation), and adequate potassium intake (3 g/day – 4 g/day), especially during adaptation, is recommended.^46,89,114 Consider use of ‘light salt’ containing potassium and sodium. Dietary sources of potassium include spinach, other leafy greens and vine fruits, e.g. tomatoes, cucumbers, zucchini (courgette) and eggplant (aubergine).

Medication interactions and adjustments may occur because of these effects (see ‘Medication and monitoring’ section).

Constipation may also be associated with inadequate fluid intake – increase to a minimum of 2 l per day. Fibre consumption (usually sufficient on a whole food TCR approach) can be explored either by increasing it (more vegetables or chia seeds and flax seeds) or decreasing it, depending on the underlying cause of constipation.¹⁰⁰ Other options include milk of magnesia (1 teaspoon) or magnesium citrate (240 mL, adult single dose, mixed with water) at bedtime,¹⁶⁸ additional sodium or a sugar-free fibre supplement (e.g. psyllium). If constipation persists, an individualised approach, examining potential triggers (e.g. an increase in the consumption of certain foods, such as nuts or cheese), may be required. Note: Reduced stool frequency can occur when reducing carbohydrate intake and may not be pathological (constipation, defined as hard, painful stools that require straining to pass, can occur because of a change in sleep rhythm, dehydration, iron supplements or the need to adjust fibre intake).

Muscle cramps are a common side effect, especially in the early days and weeks after initiating a low-carbohydrate diet, also influenced by electrolyte imbalance. Magnesium supplementation can be supportive if attention to hydration and sodium is insufficient. Ensure there are no contraindications to use, e.g. impaired renal function, pregnancy or neuromuscular disease.¹⁶⁹ Options include slow-release magnesium chloride or magnesium glycinate (magnesium bisglycinate), supplying 200 mg – 400 mg of elemental magnesium daily. Magnesium glycinate is well absorbed and is less likely to cause gastrointestinal symptoms. Dosage can be decreased to 200 mg/day for maintenance.

Other suggestions include a spoonful of pickle juice or yellow mustard. The mechanism is not fully understood but is thought to occur via an inhibitory oropharyngeal reflex.¹⁷⁰ If muscle cramping increases with exercise or activity, use of a foam roller may benefit.

A temporary rise in LDL-c may be observed during weight loss as a physiological response to fat mobilisation and the shift in metabolism. Often LDL-c decreases or returns to baseline.^184,185

In general, low-carbohydrate diets have been shown to be effective at increasing HDL-c and decreasing triglyceride (or triacylglycerol [TAG]) with minimal change in LDL-c or total cholesterol.¹¹ In addition, studies show improvements in low-density lipoprotein (LDL) particle number and atherogenic profile using TCR approaches.^73,186 However, some uncertainty remains until CVD outcome studies are performed.

Recent data have identified the ‘lean mass hyper-responder’ (LMHR) phenotype, which may develop as weight loss occurs or in lean individuals adopting a low-carbohydrate approach for other health reasons.¹⁸⁷ In this population, these data indicate that a lower BMI tends to promote the phenotype.^187,188 Typically, these individuals are metabolically healthy with cholesterol readings defined as LDL-c ≥ 200 mg/dL (≥ 5.2 mmol/L), HDL-c ≥ 80 mg/dL (≥ 2.1 mmol/L) and TAG ≤ 70 mg/dL (0.8 mmol/L). It is still to be determined if these findings represent an increased risk for CVD in the context of good metabolic health and low inflammation, but early data have shown no association between LDL-c and plaque burden.¹⁸⁹ Consider cardiac imaging to monitor and/or stratify risk.^190,191

The cholesterol response to TCR is heterogeneous, and the interpretation of LDL-c changes requires consideration in context with an appropriate clinical assessment (lipid panel, subfractions, imaging and other metabolic health markers). Cholesterol profiles may be altered (LDL-c tends to reduce) by increasing carbohydrates (from starchy vegetables or fruit) to 50 g/day – 100 g/day, which may have a role as determined on a case-by-case basis.¹⁸⁷ TCR may be adjusted as clinically indicated according to individual responses and can accommodate a broad range of dietary patterns.

Carbohydrate reduction for metabolic disorders emphasises a wide variety of plant and animal foods with high nutrient density and will provide good nutrition for the majority of individuals.^192,193 Our current food environment, high in ultra-processed foods, may promote nutritional deficiencies in individuals, and baseline testing for nutritional deficiencies may be required. Globally, deficiencies in iron, vitamin A and iodine are the most common, particularly among children and pregnant women.¹⁹⁴ Individuals following a vegan or vegetarian dietary pattern may be more at risk of iron deficiency. Symptoms suggestive of a nutritional deficiency should be investigated.

Clinical experience suggests vitamin D and zinc are commonly deficient. Vitamin B12 and folate testing may be needed (especially if patients take metformin). However, methylmalonic acid and total homocysteine may be important to accurately diagnose a B12 deficiency.¹⁹⁵

Omega-3 long-chain polyunsaturated fatty acids (PUFAs) are essential to our diet, as they cannot be synthesised endogenously and are required for many biological functions associated with reducing inflammation, modulating lipid metabolism, brain function and neuroprotection.¹⁹⁶ Dietary sources of omega-3 PUFAs primarily come from fatty fish, and the Dietary Guidelines for Americans recommend 2 servings of fish per week. Other dietary sources include leafy greens, seeds and nuts, but, in general, omega-3 PUFAs are less common in the diet compared to omega-6 PUFAs, and supplementation may be required for sufficiency.¹⁹⁷

Magnesium is an essential mineral that recent research has implicated as a cofactor for over 600 enzymes involved in metabolism, including protein synthesis, nerve transmission, muscle function and glucose and insulin metabolism.¹⁹⁸ This mineral is commonly underconsumed (impacted by soil depletion and food processing) and is implicated in glucose control. Low-carbohydrate sources of magnesium (if tolerated) include dark green vegetables, nuts, seeds, unprocessed meats and homemade broths.¹⁹⁹

In cases of calcium deficiency, sources include dairy foods, particularly hard cheeses, which are commonly consumed on reduced-carbohydrate diets. Other sources of calcium include small fish with bones (e.g. sardines), nuts and seeds, tofu and homemade bone broths. The recommended dietary allowance for calcium in adults is 1000 mg/day – 1200 mg/day.¹⁹⁹ If patients are at risk, e.g. osteoporosis, and are not getting adequate dietary calcium, a supplement, such as calcium citrate (with vitamin K2), may be considered.²⁰⁰ In this setting, vitamin D adequacy should also be considered, as it increases intestinal absorption of calcium.²⁰¹