People with Type 1 Diabetes in the early years might be more sensitive to insulin. Still, as time progresses, (over roughly ten years), some degree of insulin resistance might accompany the condition. (there are useful publications on that) It might be the case that people with Type 1 Diabetes and insulin resistance (sometimes called double diabetes), will notice that their insulin takes longer to act after injection because of insulin resistance. On a lower carbohydrate diet, the metabolic changes caused by the reduced insulin requirements will tend to restore insulin sensitivity. The patient will begin to notice that their insulin appears more ‘potent’ in that it will act more quickly and also that they will need reduced insulin doses over and above what would be required by the dietary carbohydrate reduction. Over time they might need to reduce their basal insulin. It can be a good idea to revise basal dosing every few months if you suspect insulin resistance.
The patient will be eating a higher proportion of their diet as fat, and this, too, can cause temporary insulin resistance until it is fully metabolised. Until the patient becomes adept at managing lower carbohydrates, it can help if fat is split relatively evenly between meals.
Cutting most carbohydrates from the diet, particularly refined sugars, can be a significant change for both the brain and body. Sugar is thought to affect the brain reward system. Some people find that giving up sugar can cause withdrawal symptoms just like those of any other substance that acts via the brain reward system. Fortunately, in the majority of people, these cravings disappear in the first few weeks; in others, it can take months or longer.
Helping the patient to understand why dietary change is necessary can help to combat cravings. Many people find that removing all sugar from the diet is their best option. There are addiction questionnaires that would be suitable for exploring a person’s susceptibility to sugar addiction. One example is the Yale Food Addiction Scale.
FEELING WEAK AND DIZZY WITH LIGHTHEADEDNESS (SOMETIMES WITH A DULL HEADACHE)
The adjustment phase to lowered carbohydrates can lead to a relative lack of sodium. This is because insulin acts to retain sodium (and with it, fluid). In most people with Type 1 Diabetes who reduce their carbohydrates, their insulin total daily will decrease, and there will be a diuresis phase as the sodium is excreted through the renal tract. Fluid replacement with water is adequate. Adding extra salt in the first two weeks might also be useful. Relatively high insulin levels might be a driver for hypertension, and reducing insulin might lower blood pressure. It is good practice to monitor blood pressure in this phase if the patient feels particularly lightheaded and consider whether to review anti-hypertensive medication, especially if the patient is taking those anti-hypertensives, which cause salt loss. And also, if they are on diuretics, especially thiazides.
Any significant change in diet will cause a temporary change in bowel habits. Fluid replacement with water is adequate. Laxatives might be needed (which one ?). But this phase does pass. At 3-4 weeks, the patient often feels much more vital than previously.
The clinician’s assessment of the patient will include having knowledge of the blood tests and status of the liver, gall bladder, pancreas, kidneys, and gut. Active disease in any digestive organ might be approached with a more cautious transition if planning very low carbohydrates. However, many of these conditions will respond well. For example, non-alcoholic fatty liver can be reversed relatively quickly on a ketogenic diet. Individual assessment is key to safe management.
Caution is also recommended in those with ‘brittle’ diabetes and hypoglycaemic unawareness. Until you can be sure that the patient has an adequate glucagon response to low blood glucose, it is not recommended to proceed with reducing carbs to a level that might pose a risk. Some people are highlighting the possibility of glucagon resistance, especially in steatohepatitis, which again should be borne in mind in Type 1.
Gall bladder disease and gallstones can sometimes worsen if the transition to very low carbohydrate is too swift. It might be prudent to plan several months of gradual weaning down to lowered carbohydrate to avoid precipitating complications.
There have been reports in children with medically intractable epilepsy, that renal calculi are recognised complications in this group managed with a keto diet. Calculus composition has been reported as uric acid, calcium oxalate, or a mixture of calcium oxalate and calcium phosphate/uric acid. It is not known if this can be translated to Type 1 diabetes, but it would be again prudent to proceed with more caution in people with Type 1 with a personal or family history of renal stone formation.
There have been rare reports of euglycemic ketoacidosis in people with Type 1 Diabetes. This is a diagnosis of exclusion with metabolic acidosis and is difficult to diagnose. It should be on the list of differential diagnoses of a Type 1 who has symptoms of DKA with normal glucose. It has been described in infection, insulin pump failure, and also when insulin is combined with an SGLT2 inhibitor. None of these patients were on a low carb diet, but there is the possibility that this could happen on all types of diet. Ketone testing should be encouraged for all people with Type 1 Diabetes when they are unwell.
People who use very low carbohydrate diets can experience asymptomatic hypoglycaemia. While this is not specific to Type 1 Diabetes, exogenous insulin on a very low carbohydrate diet might add a further complicating dimension to this phenomenon. If someone with Type 1 can access a CGM, it will make not only this but also all other aspects of management much more relaxed.
There are medical conditions that do not suit a low carbohydrate diet down to ketogenic levels. These are mainly inherited disorders of lipid metabolism, pyruvate carboxylase deficiency, plus porphyria.
For people with advanced diabetes complications, it is crucial to manage the transition with great care. In some situations, as we know, improvement of diabetes control can temporarily worsen complications. The body has taken years to get to the state of advanced diabetes and will have tried to adapt to high blood glucose levels by storing excess glucose as fat or urinating out glucose. Not to mention the insulin resistance brought about by chronic insulin overdosing, and vagal neuropathy. A rapid transition to ketone metabolism could possibly upset that balance. So, the risk: benefit has to be balanced carefully. Very small steps might work, or it may be that the risk is too high, and it might be best to revert to the patient’s usual regimen if it seems safer to do so.