The 5 Necessities of an Effective Weight Loss Diet for People With Diabetes


weight loss for people with diabetes

This is not just another general “eat salad and completely avoid carbs” article. I’m tired of seeing generalized diet information that, to be brutally honest, is pointless and inapplicable to most people’s lives. This article is aimed to help the diabetic community focus on and prioritize what works.

Weight loss is science, not magic or voodoo or luck. There is a specific set of requirements needed to lose weight efficiently as a person with diabetes (type 1 or type 2). Yes, you may have heard of your friend’s cousin’s mother doing a no carb detox cleansing bath scrub to lose belly fat who lost 10 pounds, but I highly encourage you to check in with that person who does every fad diet possible in a few weeks or months. Chances are they gained the weight back and then some.

That’s because while some diets cause people to lose weight initially, they don’t employ the basic principles of continued effective weight loss. Whether it’s water weight loss, weight loss from severe calorie deficit, or avoidance of food, a lot of diets promise and sometimes produce acute results — that is temporary or short term results.

From helping hundreds of diabetics lose weight on social media, I was nicknamed the “T1D Fat Loss Coach” and now help people with all kinds of diabetes and chronic illnesses get on effective diets.

I have a 3 “E” rule for an effective diet before you continue on in this article. A diet must be all three of the following for you for it to be effective:

  1. Easy to adhere to long term
  2. Enjoyable or at least not miserable and affecting quality of life (socially or mood related)
  3. Effective in producing results long term (any diet change can produce short term results)

So, in deciding on a diet, make sure you have these rules in mind. These next five components of a diet will determine your success.

Optimal Weight Loss Blood Sugar

Blood sugar management is more important than exercise and diet combined for weight loss. Why? Because chasing blood sugars involves ruining your diet and training effectiveness.

You can’t optimally lose fat, build lean muscle, or get a healthier physique while mismanaging your blood sugars.

When your sugars are low, you are likely to (or at least more at risk to):

  • Overeat to correct lows
  • Overcompensate the overeating with medication that could lead to another low
  • Experience another low in the next 24-48 hours (“lows beget lows”)
  • Reduce intensity of exercise
  • Experience increased hunger and cravings which can be hard to fight

When your blood sugars are high, you are likely to (or at least more at risk to):

  • Overtreat with insulin which could lead to another low
  • Reduce nutrient absorption necessary to increase or preserve lean muscle mass
  • Decrease effectiveness of a workout
  • Experience a false sense of scale weight loss when in reality, you could be losing lean tissue which means reducing your metabolic rate and storing more body fat

In order to improve your metabolic rate and your body’s fat burning capability/processes, blood sugar management has to be a priority. In order to reduce cravings and hypo and hyperglycemic events that negatively affect diet and training, blood sugar management must be a main priority that isn’t overlooked.

Talk to your endocrinologist and diabetes management team as you decide on what the best approach is in conjunction with your changing diet and exercise habits. Then, you can get into specifics on calories and the makeup of those calories for fat loss optimization.

Specifying Calorie Intake

In order for you to lose weight, you have to be in a calorie deficit — that means burning more calories than you take in. You can do this by eating less, burning more calories through activity, or, ideally, a combination of both.

But first, you have to determine what is the appropriate number of calories you should be intaking based on your personal stats and goals. But can’t I just eat “healthy” and lose weight? You can and leave it to chance but even if you eat healthy foods in the wrong quantities, you will gain weight.

There is no universal fix to an individual problem.

That means what works for me doesn’t optimally work for your mom or for you. Specificity is optimal. To figure out how many calories you need to consume, you can find any TDEE calculator online like this one. This determines your Total Daily Energy Expenditure, or the calories you need to eat to maintain your current weight.

 IIFYM TDEE calculator

Now if you want to lose weight, you need to be in a caloric deficit which means you need to eat less than what you expend daily. My personal, general rule of thumb is:

  • If you want to lose 5 lbs/2 kg or less, subtract 250 calories from your TDEE
  • If you want to lose 5-15 lbs/2-7 kg, subtract 500 calories from your TDEE
  • If you want to lose over 20 lbs/10 kg, subtract up to 750 calories from your TDEE

This is a general rule that has helped hundreds of my type 1 and type 2 online weight loss clients lose between 5-60 lbs/2-25 kg but always be sure to consult your doctor before starting a new diet and training program.

Once you have your daily caloric limits, you can be more specific and determine your macronutrient goals.

Identifying Your Ideal Macro Balance

Calories determine weight change, but macronutrient balance determines the kind of weight change. Macronutrients are your proteins, carbohydrates, and fats.

  • Protein has 4 calories per gram
  • Carbs have 4 calories per gram
  • Fat has 9 calories per gram

Why is macronutrient balance important? Take two people eating a 1500 calorie diet based on the advice above. Person A is eating 90% fat, 5% carbs, and 5% protein while person B is eating a balanced macronutrient diet of 35% protein, 30% carbs, and 35% fat. Who will get better results?

Person A is eating far too little protein and far too much fat. Higher protein diets are effective in helping people lose body fat, reduce hunger and cravings, and manage blood sugars. That little protein intake would increase risk of lean muscle loss which is the exact opposite goal. High protein diets are also proven to not be dangerous or harmful to the kidneys as long as there is no pre existing kidney damage.

That high of fat intake might make person A more hungry too as fat is more calorie dense meaning less total food intake. More hunger = more of a chance to fall off the diet when faced with opportunity to cheat.

The goal is to preserve or even build lean muscle while losing body fat. Losing muscle decreases your metabolic rate and lowers your body’s ability to burn fat. Keeping your protein around 30-40% of your total caloric intake is key for long term fat loss.

What about carbs?

Given that protein is 30-40%, carbs I leave up to my clients’ personal preference. Some people choose a moderate carb intake, some choose a lower carb intake, and some even choose to follow a ketogenic approach.

I personally don’t care as long as you are managing your sugars, eating the right protein amount, and hitting around your decided macronutrient intakes.

In terms of pure weight loss science, hundreds of studies have compared low-carb, high-fat diets to high-carb, low-fat diets and found no significant difference in weight loss when calories and protein are equated.

There may be some instances where clients with insulin resistance or hormonal issues (Type 2, PCOS, Hashimotos, post menopause, etc.) might be encouraged to be on the lower side of carb intake but, for the most part, it is a personal choice.

Carbs and fats usually have an inverse relationship — if one is higher the other is lower. If your protein intake is at 30% and you decide you want to do a moderate carb approach at 30% carbs, then you know your fat intake will be 40% (the remainder).

Some of my preferred macro percentages with my clients are:

  • Low-carb: 40% protein/20% carbs/40% fat
  • Moderate carb: 35% protein/30% carbs/35% fat
  • Moderate carb, high activity level: 40% protein/30% carbs/30% fat

These are just a few of the many possibilities and strategies to elicit fat loss. Simply download a calorie counting app like My Fitness Pal to track these numbers discussed above.

Navigating My Way Through a Food Heavy Culture

Food Choices

It is not necessarily the choices of food that affect us as much as the quantities of food in terms of weight gain and weight loss, directly speaking. Indirectly, food choice can be a major indicator of adherence to a diet.

Eating processed foods is shown to decrease satiety (feeling of fullness), increase cravings, and increase guilt. These repercussions of not eating healthy can slow or even reverse progress. I like to take an 80/20 approach with my diabetic clientele and myself.

80% of the food eaten should be whole foods. 20% can be your personal indulgent. That means if you are alloted 1500 calories a day, 20%, or 300 calories, can come from your craving foods. I believe this helps people cheat within the diet so they stay on track for longer and get far better results than being extremely strict.

An interesting note, a Kansas state nutrition professor ate twinkies and protein shakes for 10 weeks and lost 27lbs/12kg and improved his metabolic profile in the process. He wanted to show that quantity of food is extremely important when it comes to weight loss. Obviously, I don’t recommend doing this and neither does he, so please don’t replicate his experiment.

Meal Timing & Frequency

One of the biggest myths in the dieting world is having to eat every two hours to “stoke the metabolic fire.” There is no metabolic fire or fire inside of your body — I promise. Daily macronutrient & caloric totals matter most not meal timing or frequency. When you add diabetes to the mix, that’s when these variables become more relevant.

Meal timing prior to cardio or exercise can determine if you are going to have a great workout or diabetic emergency. Both hypo- & hyperglycemia can ruin a workout so timing meals according to your activity level can greatly improve blood sugar management, which indirectly improves your ability to adhere to your diet and training.

Meal frequency is a personal preference but some people with diabetes find it easier to minimize glucose variability with smaller, more frequent meals. Ultimately, that is your decision. Whatever fits into your lifestyle best is what you should do.

Effective Weight Loss With Diabetes

Blood sugar management, proper caloric intake, and macronutrient balance will help you lose body fat long term, the right way. There are tons of advanced strategies I’ve used to help people with diabetes transform their bodies but all progress stems from these basic principles. Yes, it takes some work. Yes, you have to type some stuff and do some math. Yes, it takes conscious, daily effort just like diabetes management. But, in doing so, your body will thank you.

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Effect of calcium-based versus non-calcium-based phosphate binders on mortality in patients with chronic kidney disease: an updated systematic review and meta-analysis.


Background

Phosphate binders (calcium-based and calcium-free) are recommended to lower serum phosphate and prevent hyperphosphataemia in patients with chronic kidney disease, but their effects on mortality and cardiovascular outcomes are unknown. We aimed to update our meta-analysis on the effect of calcium-based versus non-calcium-based phosphate binders on mortality in patients with chronic kidney disease.

Methods

We did a systematic review of articles published in any language after Aug 1, 2008, up until Oct 22, 2012, by searching Medline, Embase, International Pharmaceutical Abstracts, Cochrane Central Register of Controlled Trials, and Cumulative Index to Nursing and Allied Health Literature. We included all randomised and non-randomised trials that compared outcomes between patients with chronic kidney disease taking calcium-based phosphate binders with those taking non-calcium-based binders. Eligible studies, determined by consensus with predefined criteria, were reviewed, and data were extracted onto a standard form. We combined data from randomised trials to assess the primary outcome of all-cause mortality using the DerSimonian and Laird random effects model.

Findings

Our search identified 847 reports, of which eight new studies (five randomised trials) met our inclusion criteria and were added to the ten (nine randomised trials) included in our previous meta-analysis. Analysis of the 11 randomised trials (4622 patients) that reported an outcome of mortality showed that patients assigned to non-calcium-based binders had a 22% reduction in all-cause mortality compared with those assigned to calcium-based phosphate binders (risk ratio 0·78, 95% CI 0·61—0·98).

Interpretation

Non-calcium-based phosphate binders are associated with a decreased risk of all-cause mortality compared with calcium-based phosphate binders in patients with chronic kidney disease. Further studies are needed to identify causes of mortality and to assess whether mortality differs by type of non-calcium-based phosphate binder.

Source: Lancet

N-Acetylcysteine Plus Intravenous Fluids Versus Intravenous Fluids Alone to Prevent Contrast-Induced Nephropathy in Emergency Computed Tomography.


Abstract

STUDY OBJECTIVE:

We test the hypothesis that N-acetylcysteine plus normal saline solution is more effective than normal saline solution alone in the prevention of contrast-induced nephropathy.

METHODS:

The design was a randomized, double blind, 2-center, placebo-controlled interventional trial. Inclusion criteria were patients undergoing chest, abdominal, or pelvic computed tomography (CT) scan with intravenous contrast, older than 18 years, and at least one contrast-induced nephropathy risk factor. Exclusion criteria were end-stage renal disease, pregnancy, N-acetylcysteine allergy, or clinical instability. Intervention for the treatment group was N-acetylcysteine 3 g in 500 mL normal saline solution as an intravenous bolus and then 200 mg/hour (67 mL/hour) for up to 24 hours; and for the placebo group was 500 mL normal saline solution and then 67 mL/hour for up to 24 hours. The primary outcome was contrast-induced nephropathy, defined as an increase in creatinine level of 25% or 0.5 mg/dL, measured 48 to 72 hours after CT.

RESULTS:

The data safety and monitoring board terminated the study early for futility. Of 399 patients enrolled, 357 (89%) completed follow-up and were included. The N-acetylcysteine plus saline solution group contrast-induced nephropathy rate was 14 of 185 (7.6%) versus 12 of 172 (7.0%) in the normal saline solution only group (absolute risk difference 0.6%; 95% confidence interval -4.8% to 6.0%). The contrast-induced nephropathy rate in patients receiving less than 1 L intravenous fluids in the emergency department (ED) was 19 of 147 (12.9%) versus 7 of 210 (3.3%) for greater than 1 L intravenous fluids (difference 9.6%; 95% confidence interval 3.7% to 15.5%), a 69% risk reduction (odds ratio 0.41; 95% confidence interval 0.21 to 0.80) per liter of intravenous fluids.

CONCLUSION:

We did not find evidence of a benefit for N-acetylcysteine administration to our ED patients undergoing contrast-enhanced CT. However, we did find a significant association between volume of intravenous fluids administered and reduction in contrast-induced nephropathy.

Source: Pubmed

 

N-Acetylcysteine Plus Intravenous Fluids Versus Intravenous Fluids Alone to Prevent Contrast-Induced Nephropathy in Emergency Computed Tomography..


Abstract

STUDY OBJECTIVE:

We test the hypothesis that N-acetylcysteine plus normal saline solution is more effective than normal saline solution alone in the prevention of contrast-induced nephropathy.

METHODS:

The design was a randomized, double blind, 2-center, placebo-controlled interventional trial. Inclusion criteria were patients undergoing chest, abdominal, or pelvic computed tomography (CT) scan with intravenous contrast, older than 18 years, and at least one contrast-induced nephropathy risk factor. Exclusion criteria were end-stage renal disease, pregnancy, N-acetylcysteine allergy, or clinical instability. Intervention for the treatment group was N-acetylcysteine 3 g in 500 mL normal saline solution as an intravenous bolus and then 200 mg/hour (67 mL/hour) for up to 24 hours; and for the placebo group was 500 mL normal saline solution and then 67 mL/hour for up to 24 hours. The primary outcome was contrast-induced nephropathy, defined as an increase in creatinine level of 25% or 0.5 mg/dL, measured 48 to 72 hours after CT.

RESULTS:

The data safety and monitoring board terminated the study early for futility. Of 399 patients enrolled, 357 (89%) completed follow-up and were included. The N-acetylcysteine plus saline solution group contrast-induced nephropathy rate was 14 of 185 (7.6%) versus 12 of 172 (7.0%) in the normal saline solution only group (absolute risk difference 0.6%; 95% confidence interval -4.8% to 6.0%). The contrast-induced nephropathy rate in patients receiving less than 1 L intravenous fluids in the emergency department (ED) was 19 of 147 (12.9%) versus 7 of 210 (3.3%) for greater than 1 L intravenous fluids (difference 9.6%; 95% confidence interval 3.7% to 15.5%), a 69% risk reduction (odds ratio 0.41; 95% confidence interval 0.21 to 0.80) per liter of intravenous fluids.

CONCLUSION:

We did not find evidence of a benefit for N-acetylcysteine administration to our ED patients undergoing contrast-enhanced CT. However, we did find a significant association between volume of intravenous fluids administered and reduction in contrast-induced nephropathy.

Source: Pubmed

 

 

Pre-eclampsia and the risk of kidney disease.


Worldwide, about 2—8% of pregnancies are complicated by pre-eclampsia, a disorder that is characterised by new-onset hypertension and proteinuria after 20 weeks of pregnancy.1 Pre-eclampsia is associated with risk of adverse fetal outcomes and can progress to severe pre-eclampsia, eclampsia, or death if not diagnosed and treated with delivery. Substantial progress in understanding the pathophysiological mechanisms of the disease has been made in recent years, and changes in concentrations of soluble fms-like tyrosine kinase 1 and other angiogenic factors seem to be key.2 However, mechanisms behind pre-eclampsia and development of acute kidney injury and chronic kidney disease in the mother are less well understood and warrant further discussion.

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Although acute kidney injury caused by pre-eclampsia or eclampsia is rare in high-income countries, it complicates 2% of third-trimester pregnancies in India, for example, with pre-eclampsia accounting for 36% of cases (ie, pre-eclampsia associated with acute kidney injury might occur in one of 150 pregnancies).3 Dialysis might be required in up to 50% of cases, and when not available, acute kidney injury is a frequent cause of maternal death. Other major causes of acute kidney injury associated with pregnancy in developing countries include sepsis and major bleeding, whereas less common disorders such as primary renal disease, thrombotic thrombocytopenic microangiopathy, or acute fatty liver of pregnancy are probably relatively more common in developed countries. Although most women with acute kidney injury in pregnancy recover renal function, 7—29% do not fully recover, which can have serious long-term outcomes.34 However, few high-quality studies have assessed the cause, prevalence, and prognosis of acute kidney injury in pregnancy, and more studies are needed to inform strategies for prevention, treatment, and follow-up.

Despite several small studies showing recovery of renal function after so-called pure pre-eclampsia,4 a population-based study from Norway suggested that women who had had pre-eclampsia were at a four-to-five-times increased risk of development of end-stage renal disease during a follow-up of 35 years.5 The risk was significant after exclusion of women with known kidney disease, diabetes, hypertension, or rheumatic disease before pregnancy. Other studies67 showed that pre-eclampsia was a significant risk marker for development of kidney disease, requiring a diagnostic kidney biopsy, but that previous pre-eclampsia was not associated with rapid progression of established kidney disease to end-stage renal disease, suggesting that pre-eclampsia is more strongly associated with the development of kidney disease than with subsequent progression. A Taiwanese study8 also noted an increased risk of chronic kidney disease and end-stage renal disease in women with previous pre-eclampsia. In line with these findings, a meta-analysis concluded that women with previous pre-eclampsia had a four-times increased risk of microalbuminuria 5—10 years after a pre-eclamptic pregnancy compared with women without previous pre-eclampsia.9 This meta-analysis was, however, restricted by inclusion of small studies of variable quality and most of the women either had severe pre-eclampsia or underlying disease such as diabetes mellitus. Associations between pre-eclampsia and subsequent microalbuminuria, which suggest renal injury resulting from pre-eclampsia, need to be verified in large population-based studies.

How pre-eclampsia predisposes to an increased risk of renal disease is not well understood. The issue is complicated by the strong association between pre-eclampsia and cardiovascular risk factors, which also increase risk of kidney disease. That pre-eclampsia might induce primary renal injury is, however, supported by reports that the risk of kidney disease and microalbuminuria after pre-eclampsia seems to be greater than the risk of cardiovascular disease.5910 In addition, much the same increase in risk was noted for all types of kidney disease after pre-eclampsia,56 underscoring the hypothesis that a primary renal insult, possibly mediated by extensive endothelial or podocyte injury,11 induces nephron loss and contributes to progression of renal disease. The strong clinical similarity between pre-eclampsia and underlying kidney disease also complicates these studies, because the clinical presentations can be almost identical, especially in multiparous women.12

Developmental and genetic factors are also important determinants of pre-eclampsia risk (as discussed in the accompanying Series), and might themselves be independent risk factors for renal disease. Men and women born in pre-eclamptic pregnancies are at an increased risk of fathering or bearing pre-eclamptic pregnancies, respectively,13 and women born with low birthweight had a 1·5-fold increased risk of pre-eclampsia.14 This intergenerational transfer of risk might suggest genetic predisposition, perinatal programming, or socioeconomic factors, the last of which is an independent risk factor for pre-eclampsia, especially in developing countries.15

Pre-eclampsia is probably an important cause of acute kidney injury and an important risk marker for subsequent chronic kidney disease. Women with previous pre-eclampsia should receive long-term follow-up, especially with respect to hypertension, insulin resistance, and obesity. However, pre-eclampsia might also unmask underlying primary renal disease, and women with pre-eclampsia should be monitored for proteinuria and hypertension within 6—8 weeks of delivery and have a nephrological work-up if these disorders do not resolve.

References

1 Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. Lancet 2010; 376: 631-644. Summary | Full Text |PDF(865KB) | CrossRef | PubMed

2 Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med 2004; 350: 672-683. CrossRef | PubMed

3 Prakash J, Niwas SS, Parekh A, et al. Acute kidney injury in late pregnancy in developing countries. Ren Fail 2010; 32: 309-313.CrossRef | PubMed

4 Sibai BM, Villar MA, Mabie BC. Acute renal failure in hypertensive disorders of pregnancy. Pregnancy outcome and remote prognosis in thirty-one consecutive cases. Am J Obstet Gynecol 1990; 162: 777-783. CrossRef | PubMed

5 Vikse BE, Irgens LM, Leivestad T, Skjaerven R, Iversen BM. Preeclampsia and the risk of end-stage renal disease. N Engl J Med2008; 359: 800-809. CrossRef | PubMed

6 Vikse BE, Irgens LM, Bostad L, Iversen BM. Adverse perinatal outcome and later kidney biopsy in the mother. J Am Soc Nephrol2006; 17: 837-845. CrossRef | PubMed

7 Vikse BE, Hallan S, Bostad L, Leivestad T, Iversen BM. Previous preeclampsia and risk for progression of biopsy-verified kidney disease to end-stage renal disease. Nephrol Dial Transplant 2010; 25: 3289-3296. CrossRef | PubMed

8 Wang IK, Muo CH, Chang YC, et al. Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ 2013; 185: 207-213. CrossRef | PubMed

9 McDonald SD, Han Z, Walsh MW, Gerstein HC, Devereaux PJ. Kidney disease after preeclampsia: a systematic review and meta-analysis. Am J Kidney Dis 2010; 55: 1026-1039. CrossRef | PubMed

10 Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre-eclampsia and risk of cardiovascular disease and cancer in later life: systematic review and meta-analysis. BMJ 2007; 335: 974. CrossRef | PubMed

11 Garovic VD, Wagner SJ, Turner ST, et al. Urinary podocyte excretion as a marker for preeclampsia. Am J Obstet Gynecol 2007;196: 320. PubMed

12 Fisher KA, Luger A, Spargo BH, Lindheimer MD. Hypertension in pregnancy: clinical-pathological correlations and remote prognosis. Medicine (Baltimore) 1981; 60: 267-276. PubMed

13 Skjaerven R, Vatten LJ, Wilcox AJ, Ronning T, Irgens LM, Lie RT. Recurrence of pre-eclampsia across generations: exploring fetal and maternal genetic components in a population based cohort. BMJ 2005; 331: 877. CrossRef | PubMed

14 Rasmussen S, Irgens LM. Pregnancy-induced hypertension in women who were born small. Hypertension 2007; 49: 806-812.CrossRef | PubMed

15 Nanjundan P, Bagga R, Kalra JK, Thakur JS, Raveendran A. Risk factors for early onset severe pre-eclampsia and eclampsia among north Indian women. J Obstet Gynaecol 2011; 31: 384-389. CrossRef | PubMed

Source: Lancet

Renal Disease Associated with Adverse CV Events in Patients with Atrial Fibrillation .


Among patients with atrial fibrillation, chronic kidney disease is associated with higher risk for adverse cardiovascular events, according to a study in the New England Journal of Medicine.

Using Danish registries, researchers compared outcomes based on renal status in roughly 130,000 patients hospitalized for atrial fibrillation.

Non-end-stage chronic kidney disease and kidney disease requiring renal-replacement therapy were associated with increased risks for stroke or systemic thromboembolism, bleeding, MI, and all-cause mortality, relative to no renal disease. Warfarin decreased the risk for stroke or thromboembolism in patients with renal disease (hazard ratio, 0.76), while aspirin was associated with increased risk (HR, 1.17).

Mark Link of Journal Watch Cardiology says: “These findings suggest that aspirin should not be routinely prescribed for stroke prevention in AF patients with renal disease, although it may still have a role in the treatment of those with coronary artery disease.”

Source:NEJM