Eating carbs last gives lower blood sugar spikes

From IDDT newsletter December 2018

A report in BMJ Open Diabetes Research and Care Sept 2017 shows that in type two diabetes, eating sugar and starch later in the meal halved the blood sugar spike after the meal compared with those who ate the sugar and starch first.

This study was done on 16 people who ate test meals of protein, vegetables, bread and orange juice. Those who were instructed to eat the bread and juice last also had 40% lower post meal glucose levels compared to those who ate all of the meal components in a mixed fashion.

My comment: This is a small study but easily reproducible with yourself and your blood glucose meter. If you do wish to eat sugar and starch best have these last, unless you are treating a hypo.

 

 

More fat = more kidney failure

From BMJ 12th January 2019

Chang AR et al The CKD Prognosis Consortium BMJ 2019;364:k5301

Between 1970 and 2017 a huge number of people were assessed for fatness using body mass index, waist circumference and waist to height ratio. The outcome was that the fatter you get, the more your kidney function declines. This was true whether you started off  with normal or impaired kidney function.

The lowest kidney disease was seen in those with a BMI of 20 and this barely changed till a BMI of 25 was reached. After this was a linear progression. By the time your BMI is 40, you have double the risk of kidney function impairment.

The results were adjusted for age, sex, race and current smoking.

My comment: This is a new risk factor for obesity as far as I know.

 

 

 

Hypoglycaemia: the neglected complication

Adapted from Hypoglycaemia: the neglected complication by Sanay Kalra et al.

Indian J Endocrinol Metab. 2013 Sep-Oct; 17(5): 819-834

Hypoglycaemia is an important complication of glucose lowering therapy in patients with diabetes mellitus. Attempts made at intensive glycaemic control invariably increases the risk of hypoglycaemia. A six fold increase in deaths due to diabetes has been found in patients with severe hypoglycaemia compared to those not experiencing severe hypoglycaemia.

Repeated episodes can lead to hypoglycaemia unawareness. Complications  of hypoglycaemia include stroke, heart attacks, cognitive dysfunction, retinal cell death and loss of vision. Apart from this there are the effects on quality of life regarding sleep, driving, employment, exercise and travel.

To maintain good glycaemic control, minimize the risk of hypoglycaemia and thereby prevent complications, there are steps that need to be taken: recognise risk factors for hypoglycaemia, use appropriate self monitoring of blood sugar, select treatment regimens that have little or no risk of incurring hypoglycaemia and teach health care professionals and patients how to avoid hypoglycaemia.

Although the DCCT showed that complications were reduced when blood sugars were brought under a HbA1C of 7%, other trials have noted a three fold risk of hypoglycaemia when the level is reduced under 6.5%. This tends to negate any improvements in long term complications.

Insulin users are most at risk. Those who have had diabetes for more than 15 years are particularly at risk. The DARTS study showed that the risk of severe hypoglycaemia was 7.1% for type one patients, 7.3% for type two patients and 0.8% for type twos on sulphonylureas. This causes increased cost for their healthcare as hospitalisation for around a week is needed in the average case.

The majority of hypos are due to medications but there are other potential causes such as: pancreatic or islet cell tumours, dietary toxins, alcohol, stress, infections, sepsis, starvation and excessive exercise.

In diabetics not eating enough food was the most common cause. Others were physical exercise, insulin miscalculation, stress, overtreating a high blood sugar, and impaired glycaemic awareness.

Nocturnal hypoglycaemia is seen in half of diabetic children, particularly under the age of 7. Dead in bed syndrome causes 5-6% of all deaths in type one youngsters.  Contributory factors are increased exercise that day or delayed meals.

In type two patients additional causative factors are alcohol ingestion and liver disease and duration of insulin over ten years. As in type ones there tends to be more hypoglycaemic unawareness as the person ages. In type twos  there is a 9 fold increase in deaths in those with hypoglycaemic unawareness.

Severe hypos in elderly patients increase the risk of dementia, functional brain failure and cerebellar ataxia. There are clear signs of neuronal death in specific brain areas at post mortem in these patients and a history of fits make these more extensive.

Hypos in elderly patients promote cardiac ischaemia. Arrhythmias are more likely due to catecholamine release during hypos. Prolonged QT intervals lead to increased heart rate, fibrillation and sudden cardiac death.  Inflammatory cytokines are released during hypos, abnormalities of platelet function and the fibrinolytic system occur.

Hypos can cause double vision, blurred vision and dimness of vision.  Blindness can occur due to retinal cell death.

Recurrent hypos make people feel powerless, anxious and depressed. Acute hypos cause mood swings, irritability, stubbornness and depression.  Quality of life scores are worse in patients with recurrent hypos.

Driving ability is affected by hypos. The affected driver can inadvertently cross lanes and speed and generally drive worse.

Hypos at night may be recognised by sleep disturbance, morning headaches, chronic fatigue and mood changes. In young children fits and bed wetting may occur.

Hypos at work can be awkward, embarrassing and frightening. Hypos are particularly dangerous for those who work at heights, underwater, on railway tracks, oil rigs, coal mines, handling hot metals or heavy machines.

Expert medical advice and planned action counselling can help workers. So can self blood glucose testing, healthy food options in canteens, flexible meal times, arrangements to carry and use emergency glucose/sugar, storage and disposal sites for medications and sharps, and time off for medical appointments. Work time and productivity due to hypos can be reduced and nocturnal hypos can also have a knock on effect the next day.

Hypos in children tend to be increased in summer months when they are more active. In adults, intense prolonged exercise following an episode of recent severe hypoglycaemia can damage skeletal muscle and the liver and can cause severe neurological symptoms.

Travelling long distances, particularly over times zones can cause insomnia, tiredness, stress, reduced appetite, nocturia,  gastric disturbance, muscle aching and headaches. Psychological symptoms include low mood, irritability, apathy, malaise, poor concentration. These deficits in both physical and mental performance can profoundly affect decision making.

The fear of hypos can affect patients more profoundly than the fear of long term complications.  Withholding of insulin can occur. Sometimes patients refuse to start it when they need it and sometimes they miss out their doses.

About 30% of type one patients are affected by hypoglycaemia unawareness and under 10% of type two patients are thus affected. Duration of insulin use is the main common factor.

Educating patients about how to detect, treat and prevent hypoglycaemia must be understandable to the patient and their family.

In 2013 the ADA recommended that insulin users test their blood sugars 6-8 times a day.

Basal insulin needs to be matched to the patients needs. If hypos persist, particularly overnight, switching to pump therapy may help.

Newer diabetic medications, which do not cause low blood sugars such as the gliptans and gliflozins, may be preferable in type two patients who have multiple co-morbidities, are elderly,  who live alone, are at high risk of falls, and who have hypoglycaemia unawareness or who otherwise could not effectively deal with a hypo.

 

 

 

Dietary calcium doesn’t make your bones stronger after all

Although it is current practice to prescribe vitamin D and calcium together, particularly in post menopausal women, a six year study shows that the added calcium has no value.

The women were all over the age of 65 and had osteopenia. This is the stage before osteoporosis. 1,994 women were randomised to take zolendronic acid or placebo.  Bone mineral density was measured at the spin, total hip, femoral neck and total body three times at intervals.

The baseline BMD was unrelated to dietary calcium after controlling for age, height, weight, physical activity, alcohol intake, smoking and past HRT use when a cross section of women were studied.

Loss of BMD over the next six years was not related to the amount of dietary calcium ingested.

Bristow SM et al. Dietary Calcium intake and bone loss over six years in osteopenic post menopausal women. J Clin Endocrinol Metab. 2019 Mar 21.

My comment: Maybe time to ditch the calcium?

And while we are on the subject of bones, I’m pleased to say that another study has shown that high dose vitamin D supplementation does NOT increase kidney stone risk.

Over just over 3 years of taking 100,000 iu of vitamin D3 each month did not increase excess calcium in the blood or the onset of kidney stones in adults aged between 50 and 84 years.

This dose is equivalent to 3300 iu vit D3 a day, similar to what many of us in the know take.

158 people took part in the randomised trial. The number of people developing kidney stones was similar in each group and no one in the intervention group developed hypercalcaemia.  The groups self reported stones. No ultrasound was done which the authors say could have been more accurate.

Malihi Z et al. Monthly high dose vitamin D supplementation does not increase kidney stone risk or serum calcium: results from a randomised controlled trial. Am J Clin. Nutr. 2019 Apr 21

 

Liraglutide can improve fatty liver damage as well as blood sugars

Adapted from Glucagon like peptide-1 receptor agonists for the management of obesity and non-alcoholic fatty liver disease: a novel therapeutic option. 

Gauri Dhir and Kenneth Cusi  Endocrinology/Metabolism Review Volume 66 Issue 1 2018

Obesity is a major risk factor for type two diabetes and a cluster of metabolic factors that lead to poor cardiovascular outcomes.  The amount of fat stored in the liver tissue closely mirrors insulin resistance and metabolic health.

Non alcoholic fatty liver disease (NAFLD) is now the commonest form of liver disease in the western world and can lead progressively to non alcoholic steatohepatitis (NASH), cirrhosis and hepatocellular carcinoma.

NAFLD is present in two thirds of obese people and promotes type two diabetes.  NASH is present in half of these. NAFLD is expected to become the most common cause of liver transplantation by 2020.

Pioglitazone and the newer drugs such as Liraglutide (Victoza) can be used, as well as various dietary therapies.

If a weight loss of 10% can be achieved, there is a significant improvement in the inflammatory process that results in cell death and fibrosis in NASH. But weight loss is difficult to achieve and maintain.  Pioglitazone can improve  NASH in two thirds of non- diabetic patients and by around half in those with diabetes or pre-diabetes.  Vitamin E has also been shown to have some success in non diabetic patients.

Liraglutide and drugs of the same class affect insulin secretion in response to meals, beta cell proliferation, inhibition of glucagon secretion, delayed gastric emptying, and making you feel fuller with less to eat.

These effects result in worthwhile clinical outcomes in overweight or obese patients whether they have diabetes or not. Body weight is reduced by at least 5% in 30% of patients and by at least 10% in 30% of patients. Over three years this can result in complete remission of the diabetes or pre-diabetes in 30% of the patients. Cardiovascular outcomes are also improved.

Triglyceride accumulation in the liver cells is the mechanism that has been recently shown to cause insulin resistant adipose tissue.  After 48 weeks of high dose Liraglutide (1.8 mg a day), resolution of NASH was seen on biopsy samples in 39% of the treated group compared to 9% in the placebo group.

The main side effects are nausea and diarrhea.  There could possibly be more gallstone development but no increase in pancreatitis.

High dose Vitamin D improves cardiovascular health markers

Adapted from UK Medical News 17 July 2018

Several different health measures, all which improve your cardiovascular outcomes, have been found to result from high dose vitamin D supplementation. You are likely to need to take at least 4,000 iu a day though, depending on how much extra sunshine you are exposed to regularly.

A meta-analysis of 81 randomised controlled trials looked at almost one thousand patients randomised to taking supplements or to a control group who did not. The active and control groups were both roughly 5,000 each.  The durations of the trials varied but averaged out at ten months. The doses ranged from 400 iu a day to 12,000 iu a day. The average taken was 3,000 iu a day.

The outcomes were related to the blood level of vitamin D achieved. Levels had to be over 86 nmol/L to get benefits. You need to take over 4,000 iu a day to get vitamin D concentrations of 100 nmol/L or more.  My comment:This does mean that the minimum levels advised by the Scottish Chief Medical Officer last year are way too low to see the benefits discussed here.

So what extra benefits do you see?

lower systolic and diastolic blood pressure.

lower high sensitivity C reactive protein.

lower serum parathyroid hormone.

lower triglycerides.

lower total cholesterol.

lower low density lipoprotein.

high density lipoprotein increased.

All benefits were numerically small but did reach statistical significance. Cardiovascular outcomes were not measured directly, only blood markers and blood pressure.

Mirhosseini N et al. Vitamin D Supplementation. Serum 25(OH)D Concentrations and cardiovascular disease risk factors: A systematic review and meta-analysis. Front Cardiovasc Med. 2018 July 12.

 

 

 

 

Metformin improves blood sugar and vascular health in type one children

 From Diabetes in Control: Metformin Improves Vascular Health in Children With Type 1 Diabetes
Nov 18, 2017
In individuals with type 1 diabetes (T1DM), cardiovascular disease (CVD) is a major issue and the primary cause of death.

Vascular changes can be detected years before progression to CVD. Targeting blood sugar regulation early in patients at high risk of developing T1DM and in those already diagnosed with T1DM, could potentially help reduce vascular dysfunction risk and even reverse changes already made in vascular function.

Past studies have shown that in adults with T1DM, metformin reduces HbA1c, BMI, and required insulin doses. It has also been suggested that metformin leads to reduced cardiovascular events and better blood sugar regulation in patients with type 2 diabetes. Studies conducted on children with T1DM suggest the same benefits. However, there is currently no research on how metformin affects vascular function in children with T1DM.
A double blind, randomized, placebo-controlled trial was conducted to evaluate the association between metformin and vascular health in children with T1DM over a 12-month period. The study included a total of 90 children from a Women’s and Children’s Hospital in South Australia.  Children were randomly divided into two groups to receive either the metformin intervention or the placebo intervention. Children who weighed 60kg or greater received 1gm of metformin twice daily and those who weighed less than 60kg received 500mg twice daily. Doses were then increased to the complete dose over a period of 2 to 6 weeks.
Follow-up was conducted at 3, 6, and 12 months from the start of the study. Vascular function was obtained at baseline and at every follow-up visit using the brachial artery ultrasound, HbA1C, insulin dose, and BMI were among some of the other outcomes measured.
Results show that vascular function defined by GTN improved over the 12-month period by 3.3% in the metformin intervention group regardless of HbA1c when compared to the placebo group (95% CI 0.3 to 6.3; P=0.03). GTN was found to be the highest in the metformin group at 3 months when compared to placebo. Children in the metformin group also experienced significant improvement (P=0.001) in HbA1c levels at 3 months (8.4%; 95% CI 8.0 to 8.8) (68mmol/mol; 95% CI 64 to 73) when compared to the placebo group (9.3%; 95% CI 9.0 to 9.7). At 12 months, the overall difference between HbA1c improvement between the two groups was lower but remained a significant 1.0% (95% CI 0.4 to 1.5) 10.9mmol/mol (95% CI 4.4 to 16.4), P=0.001. In addition, it was found that children in the metformin group had a decreased insulin dose requirement of 0.2 units/kg/day throughout the 12-month period compared to those in the placebo group (95% CI 0.1 to 0.3, P=0.001).
The following study determined that children with T1DM with above average BMIs and taking metformin saw a significant improvement in vascular smooth muscle function compared to those not taking metformin. The study suggested that in addition to vascular health, metformin also improved HbA1c levels and reduced total daily insulin dose. It was found that improvements in both vascular function and HbA1c were the highest at 3 months. This is most likely due to medication adherence being the highest around 3 months.
Practice Pearls:
In children with above average weight and who were diagnosed with type 1 diabetes, metformin provides a significant improvement in vascular smooth muscle function.
Metformin provides a significant improvement in HbA1c levels in children with type 1 diabetes.
In addition to vascular health and HbA1c benefits, metformin further aids in reducing daily insulin dose in children with type 1 diabetes.
Reference:
Anderson JJA, Couper JJ, Giles LC, et al. Effect of Metformin on vascular function in children with type 1 diabetes: A 12 month randomized controlled trial. 2017. J Clin Endocrinol Metab. 2017; 0: 1-16.