Investigating the Link Between Sugar and Obesity

Is there a link between high sugar consumption and heart disease? Increased sugar intake has been linked to obesity but this link has remained a contentious debate over the past 40 years. Recently there has been a systematic review of the literature on the association between sugar consumption and body weight. The review found that an increase or decrease in sugar intake results in parallel changes in body weight over a period of time. A similar systematic review recently published looked at total body fat intake and led to similar conclusions.

Consumption of sugar leads to an increase in postprandial plasma glucose, increases insulin concentration and reduces the concentration of HDL cholesterol. It has been suggested that sugar increases body weight by overconsumption of energy, leading to recommendations that sugar intake should be limited. In 2003 the WHO recommended that sugar intake should be limited to 10% of energy intake.  Currently in the UK it is thought that this is approximately 15%.

Sugary drinks are thought to be a major culprit because they do not result in satiety in the same way which solid sugary food does, making overconsumption easier. Glucose and fructose are also perceived to be dangerous however their composition is almost identical to sucrose. Many strchy products with high levels of carbohydrates have metabolic effects comparable to sugar. The actions needed which have been put forward include not only reduction in sugar intake but also improving the quality of carbohydrates (reducing intake of refined grain and potato products).  Sugary drinks are probably the most significant and recent measures have been employed in an attempt to reduce the volume of sugary drinks sold (eg. the ban of ‘super-sized’ fizzy drinks in New York). In my experience patient diet is often not asked about routinely during medical admissions but we could be missing out on a valuable opportunity to offer significant lifestyle advice next time a patient presents with ischaemic heart disease or complications of diabetes.

Myaesthenia Gravis – A diagnosis easily missed?

A 78 year old man who has been previously well presents with a 6 month history of double vision and drooping of his eyelids towards the end of the day. On examination he has restricted eye movements and fatiguable ptosis. CT scan of the thorax is normal. EEG confirms the diagnosis of myasthenia gravis (MG) and he is commenced on treatment with pyridostigmine.

MG is an autoimmune disorder and it is characterised by fatiguable weakness. It is mediated by antibodies against postsynaptic acetylcholine receptors and approximately 10% of patients present with a thymoma. Symptoms may worsen in heat, times of stress, pregnancy and post-partum and it is typically proximal, with the upper limbs more affected than the lower limbs. Weakness becomes generalised in aproximarely 80% of patients. Bulbar weakness can manifest as difficulty in chewing or slurred speech. The most serious complication is a myaesthenic crisis where the patient develops respiratory failure and requires mechanical ventilation. Red flags for an impending crisis include worsening of symptoms, tachypnoea, tachycardia and respiratory infection.

Symptoms of MG can be fluctuating in the initial stages, leading to this diagnosis being easily missed. The incidence in older people in particular is thought to be greater than previously perceived but it is important to diagnose the condition because it is treatable. Management of the condition involves acetylcholinesterase inhibitors for short term symptomatic relief, and oral steroids (which may initially exacerbate symptoms). Second line immunosuppressive therapies such as methotrexate or rituximab may be used and IV immunoglobulin or plasma exchange are reserved for treatment of myaesthenic crisis. Thymectomy should always be performed if a thymoma is suspected.  Patients should be councelled not to abpruptly discontinue their medication and in those undergoing surgery a dose increase  may be required.  Aminoglycosides, quinine antibiotics and IV magnesium are contraindicated in patients with MG as these drugs may impair neuromuscular transmission.