Carb Overload: Keto Sickness And Instant Carb Intake

The ketogenic diet is a popular, very low-carbohydrate, high-fat, and moderate-protein diet. While it is considered safe for most people, it can cause some unpleasant side effects, such as nausea, constipation, headaches, fatigue, and sugar cravings. These symptoms are often referred to as the keto flu and are caused by the body's withdrawal from carbohydrates and subsequent transition to burning fat for energy, also known as ketosis. When transitioning out of ketosis, some people may experience carbohydrate intolerance, where their bodies have difficulty metabolizing carbohydrates due to temporary insulin resistance. This can lead to abdominal pain, bloating, gas, diarrhea, constipation, and fatigue. Feeling sick after consuming carbohydrates could also be a sign of citrin deficiency, where patients tend to avoid high-carb foods and prefer high-fat or high-protein alternatives.

Keto flu

The keto flu is a collection of symptoms that some people experience when they start a ketogenic diet. The ketogenic diet is very low in carbohydrates, high in fat, and moderate in protein. This drastic reduction in carbohydrates can come as a shock to the body, causing withdrawal-like symptoms similar to those experienced when weaning off an addictive substance.

The keto flu can begin within the first day or two of removing carbs from your diet, and it can last a week or less for most people. However, in extreme cases, it can last up to a month. The symptoms of keto flu include:

• Stomach aches or pains
• Nausea
• Dizziness
• Sugar cravings
• Cramping
• Muscle soreness
• Irritability
• Diarrhea or constipation
• Trouble falling asleep or staying asleep
• Poor focus and concentration
• Brain fog
• Headaches
• Fatigue

To manage keto flu symptoms, it is recommended to:

• Drink plenty of water to stay hydrated and help with headaches and energy levels.
• Take an electrolyte supplement to add plenty of electrolytes like salts, potassium, and magnesium to your diet, which can help with cramps and nausea.
• Consume enough healthy fats, as low calories can lead to keto flu symptoms.
• Get plenty of rest to help with sleep issues.
• Try light exercise, such as restorative yoga, to help relieve muscle pain and tension and boost your mood and motivation.

It is important to note that the keto flu is not a medically recognized term, and if you feel very ill, you should consider visiting your doctor to rule out other causes.

Carb flu

The keto flu, also known as the "carb flu," is a collection of symptoms experienced by some people when they drastically reduce their carbohydrate intake, typically when starting a ketogenic diet. This dietary shift can cause the body to go into ketosis, a metabolic state where it burns fatty acids for energy instead of carbohydrates (glucose).

The keto flu can cause various flu-like symptoms, including:

• Stomach aches or pains
• Nausea
• Dizziness
• Sugar cravings
• Cramping
• Muscle soreness
• Irritability
• Diarrhea or constipation
• Trouble sleeping
• Poor focus and concentration
• Brain fog
• Headaches
• Fatigue

These symptoms are essentially the body's response to withdrawing from carbohydrates. They typically begin within the first few days of removing carbs from the diet and can last from a few days to several weeks, and in extreme cases, even up to a month. However, some people may never experience the keto flu, as they are naturally "metabolically flexible."

To manage keto flu symptoms, it is recommended to:

• Ease into the ketogenic diet gradually, starting with a typical low-carb diet and giving the body time to adjust.
• Stay hydrated by drinking plenty of water, as dehydration is a common issue when reducing carb intake.
• Take electrolyte supplements or increase salt intake, as an extremely low-carb diet can deplete electrolytes, leading to symptoms like cramps and nausea.
• Consume enough healthy fats and calories to prevent cravings and keep energy levels stable.
• Get plenty of rest and avoid strenuous exercise, opting for lighter activities like yoga or walking.

Insulin resistance

The complex etiopathogenesis of this dysmetabolic pandemic involves a dangerous mix of physical inactivity and unhealthy dietary patterns. Regarding physical inactivity, it has been reported that about one-third of adults worldwide fail to achieve the recommended activity levels. Thus, about 7 to 8% of all-cause and cardiovascular disease deaths are attributable to physical inactivity. This substantial non-communicable disease burden of physical inactivity is a common feature for high, middle, and low-income countries and, together with unhealthy diet, may also explain the increase in insulin resistance all around the world.

The epidemiology of isolated insulin resistance (not associated with other criteria necessary to define metabolic syndrome) shows different distributions among countries, with prevalence varying from 44.8% in a cohort of young adults in the US, 46.5% in Venezuelan adults, to 15.5% to 48.11% in Europe, depending on which population was analyzed.

One of the more promising nutritional approaches to improve insulin resistance is the ketogenic diet (KD). The KD is a diet in which the amount of carbohydrate is limited to less than 50 g per day, while the intake of fat is increased to assure an adequate energy intake. Indeed, many studies have shown a favorable effect of KD on insulin resistance in subjects with overweight or obesity. However, some studies observed a significant improvement in insulin sensitivity in response to low-carbohydrate diets even in the absence of weight loss.

The restriction in carbohydrate intake decreases intestinal absorption of monosaccharides, leading to reduced postprandial glycemia, decreased insulin requirements from the pancreas, and lower insulin levels and insulin-to-glucagon ratio. The effectiveness of the KD in lowering fasting blood glucose was confirmed in a recent meta-analysis including type 2 diabetes patients, which showed a decrease of about 1.29 mmol/L in fasting blood glucose and 1.07 in glycated hemoglobin (HbA1c). The KD also improved lipid metabolism, with significant reductions in triglycerides and total cholesterol and significant increases in HDL-c. Notably, the therapeutic effects of the KD occurred despite the duration of the intervention, which ranged from 1 to 56 weeks.

The effect of KD on insulin sensitivity appears to also be mediated by other factors than the weight loss itself. Between the raw effect of weight loss and the direct effects of ketosis on insulin resistance, there is a "middle-ground" where the effects of KD on insulin resistance may be modulated by the different effects of ketosis on fat tissue.

It is well known that visceral fat affects insulin sensitivity to a greater extent compared to subcutaneous fat. As a matter of fact, the increase in visceral lipids is associated with an increased availability of bioactive lipids, such as fatty acyl-CoAs, diacylglycerides, and ceramides that induce subclinical inflammation and insulin resistance, and a reduction in visceral adipose tissue can lead to an improvement in the metabolic health and thus of insulin sensitivity. Data from our and other labs showed unequivocally that KD are capable of significantly reducing the amount of visceral adipose tissue depots both in sedentary and active/athletic subjects. Moreover, at least in animal models, KD reduce adipose tissue cell size.

Ketogenic diets act on skeletal muscle with an "exercise-type" mechanism. It has been demonstrated that a KD, together with exercise, is able to improve skeletal muscle mitochondrial capacity and efficiency, optimizing fat oxidation and improving metabolic health markers.

Non-alcoholic liver fat disease (NAFLD) is strictly related to other metabolic diseases, such as type 2 diabetes mellitus, which, in turn, plays a pivotal role in the pathogenesis and progression of NAFLD. Consequentially, in recent years, a growing body of evidence has shown a rapid and marked reduction in liver fat accompanied by a marked decrease in body weight in NAFLD patients treated with KD. The decrease in hepatic triacylglycerol improves hepatic insulin resistance, reducing excessive hepatic glucose production and compensatory hyperinsulinemia. The lower levels of glucose and insulin in KD also reduce the cholesterol biosynthesis mediated by β-Hydroxy β-methylglutaryl-CoA reductase, which is activated by insulin. In regard to LDL-c, KD promote shifts in the particle to a larger size, decreasing the proportion of small, dense, and more atherogenic LDL particles.

A recent study showed that only 6 days of a low-calorie KD were able to decrease the intrahepatic triglyceride content of NAFLD individuals by 30% and markedly improve insulin sensitivity, which was determined by decreases in fasting serum glucose and insulin, C-peptide concentrations, and HOMA-IR. The reduction in hepatic triglycerides content despite an increase in free fatty acids concentration was attributed to an increased triglycerides hydrolysis mediated by lower insulin levels. Additionally, the increased triglycerides hydrolysis toward β-oxidation and subsequently ketogenesis was attributed to increased hepatic mitochondrial redox state.

Considering the difficulty of dissecting the effect of weight loss from that of ketosis, these results should be considered with caution. Indeed, Kirk et al. reported a similar degree of weight loss and intrahepatic triglyceride reduction in obese NAFLD patients comparing results after 11 weeks of KD vs. a control diet equivalent in calories. Similarly, a 2-week very low-calorie KD reduced both liver triglycerides (by ~55%) and body weight (−4.6 kg) in obese subjects with NAFLD, with a greater decrease in hepatic triglyceride content in the very low-calorie KD group.

Carbohydrate intolerance

Each person has their own unique carbohydrate tolerance. If you have insulin resistance, your body has difficulty dealing with carbohydrates and keeping blood sugar levels normal. The body doesn't respond normally to carbohydrate intake, and a higher carbohydrate intake only worsens the problem.

Common symptoms of carbohydrate intolerance include:

• Erectile dysfunction
• Frequent urinary or vaginal infections
• Neuropathy (tingling and numbness in your hands and/or feet)
• Weight gain, particularly around your waist
• Darker skin around your underarms, neck and skin folds

If you are carbohydrate intolerant, it is important to be cautious of your carbohydrate and sugar intake. Even foods that are usually considered “healthy”, like potatoes, oatmeal and brown rice, can raise your blood sugar and be a challenge for those who are carbohydrate intolerant.

• A low-carbohydrate diet is one of the best-studied methods for reversing diseases related to carbohydrate intolerance, such as prediabetes, type 2 diabetes and obesity.
• FODMAPs (Fermentable Oligo-Di- and Monosaccharides and Polyols) are short-chain carbohydrates found in certain foods that are resistant to digestion. A low FODMAP diet can be incorporated to combat the symptoms of carbohydrate intolerance.
• Incorporate more lean proteins and high-quality fats like olive oil, avocados, nuts, and seeds. These nutrients slow digestion and absorption, which allows for a more stable rise in blood sugar when eating carbohydrates.
• Fermented foods like kefir and sauerkraut, in addition to probiotic supplementation, can improve gut health and your body’s ability to break down carbohydrates more efficiently.

Citrin deficiency

• Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD)
• Failure to thrive and dyslipidemia caused by citrin deficiency (FTTDCD)
• Recurrent hyperammonemia with neuropsychiatric symptoms in citrullinemia type II (CTLN2)

NICCD

Children under one year with NICCD have a history of low birth weight, growth restriction, and transient intrahepatic cholestasis, hepatomegaly, diffuse fatty liver, and parenchymal cellular infiltration associated with hepatic fibrosis, variable liver dysfunction, hypoproteinemia, decreased coagulation factors, hemolytic anemia, and/or hypoglycemia. NICCD is generally not severe, and symptoms often resolve by age one year with appropriate treatment, although liver transplantation has been required in rare instances.

FTTDCD

Beyond age one year, many children with citrin deficiency develop a protein-rich and/or lipid-rich food preference and aversion to carbohydrate-rich foods. Clinical abnormalities may include growth restriction, hypoglycemia, pancreatitis, severe fatigue, anorexia, and impaired quality of life. Laboratory changes include dyslipidemia, increased lactate-to-pyruvate ratio, higher levels of urinary oxidative stress markers, and considerable deviation in tricarboxylic acid (TCA) cycle metabolites.

CTLN2

Presentation is sudden and usually between ages 20 and 50 years. Manifestations are recurrent hyperammonemia with neuropsychiatric symptoms including nocturnal delirium, aggression, irritability, hyperactivity, delusions, disorientation, restlessness, drowsiness, loss of memory, flapping tremor, convulsive seizures, and coma. Symptoms are often provoked by alcohol and sugar intake, medication, and/or surgery.

Treatment

The most successful treatment for citrin deficiency is liver transplantation. Other treatments include:

• Administration of arginine (5-10 g/day) to decrease blood ammonia concentration
• Reducing calorie/carbohydrate intake and increasing protein intake to ameliorate hypertriglyceridemia
• Administration of sodium pyruvate (4-9 g/day) to decrease the frequency of hyperammonemic episodes and improve growth
• Administration of MCT oil (45 mL/day) to aid recovery

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