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.
