While fruit can definitely be part of a healthy diabetes diet, it’s important to know the differences between the fruits you’re choosing. A handful of blueberries will have a much different impact on your blood sugar than a handful of grapes.
In this article, we’ll look at the types of sugar in fruit, which fruits raise blood sugar levels the most, and which fruits raise blood sugar levels the least.
What’s the sugar in fruit: fructose, glucose, or sucrose?
We’re often taught that all fruit contains “fructose” versus “sucrose” and that this means it’s better for our blood sugar levels. But the truth is that fruit contains a combination of fructose, sucrose, and glucose.
Fructose in small amounts (such as from a piece of fruit) is well processed by the liver and thus does not impact your blood sugar — so it’s true that many fruit choices have less impact on your blood sugar than white table sugar (sucrose). However, it’s the content of glucose in a fruit that matters most.
In the chart below, you’ll see that cherries and grapes contain significantly more glucose than berries and apples, and then bananas. But you’ll see that bananas and apples (which can also raise blood sugar levels) also contain a great deal of sucrose.
*The values in the chart are based on the Nutritionist V Database.
What about high-fructose corn syrup?
When it comes to high-fructose corn syrup, the reason it’s significantly different than fruit-derived fructose is that the amount of processed fructose is a direct cause of fatty liver disease and high triglyceride levels.
These are both components of health that increase a person’s risk for type 2 diabetes and other metabolic diseases.
A recent study reviewed by theUniversity of South Carolinaexplained that “countries that use high-fructose corn syrup in their food supply had a 20 percent higher prevalence of diabetes than countries that did not use it,” along with a “significantly increased prevalence of diabetes” despite lower rates of obesity.
So, when reading the ingredients on a packaged item, don’t confuse high-fructose corn syrup with its more natural form of simple “fructose.”
Fructose is what is found in whole, real fruit — not a packaged product or soda or candy.
5 fruits that will raise your blood sugar the most
Just because a type of fruit is on this list does not mean you can’t eat it. However, when choosing the fruits on this list, it’s important to keep an eye on just how much you’re eating.
In general, if you’re trying to avoid fruits that contain the most carbohydrates that will impact your blood sugar, aim for berries of all kinds!
Here are 5 fruits to eat with careful consideration and extra attention to your blood sugar:
“I like to call grapes ‘sugar bombs,’” says Jennifer Smith, RD & CDE from Integrated Diabetes Services.
Grapes actually top the chart of fruits containing the most total sugars. A mere 5 or 6 individual grapes can impact your blood sugar as if you just ate 2 apples.
Cherries are so fun to eat but you’ll want to be careful because it’s easy to consume 10 or 15 in a snacking moment — and they definitely impact your blood sugar.
Ranking second on the list of total sugars, 1 cup of sweet, raw cherries can pack 23 grams of total carbohydrate and 20 grams of net carbs. But if you picture how many whole cherries fit in one cup…it’s only 4 or 5 actual cherries!
Bananas are often thought of as the healthiest fruit for your blood sugar because they have a reputation of being a “complex carb” versus a “simple carb” like grapes — but bananas contain both complex and simple cars.
1 medium banana contains about 27 grams of total carbohydrate and 24 grams of net carbs. The only difference is that they might take a little longer to raise your blood sugar compared to a fruit like grapes.
You know that delicious tart flavor of pineapple? That’s partly a reflection of its very sweet sugar content.
Also a common source for juice, pineapple is a very sugar-heavy fruit choice, with 1 cup of cubed pineapple containing 22 grams of total carbohydrate and 20 grams of net carbs. In fact, one of those teeny tiny cans of pineapple juice could easily treat two low blood sugars. Super sweet!
Dried fruits (of any type)
When it comes to diabetes and eating dried fruits — watch out. The carb-count in dried fruit is no joke.
Raisins, for example, are often touted as a healthy alternative to chocolate chips when baking cookies — but a 1/2 cup of raisins contains 57 grams of total carbohydrate and 55 grams of net carbs. Sugar that’s about 12 grams less than chocolate chips but it’s still a whopper of a snack compared to eating fresh fruit.
Do keep in mind — when eating any dried fruits — that many have added sugars to compensate for tartness. Cranberries are rarely served or packaged without added sugars.
When it comes to blood sugar management, eating the fresh fruit version is almost always going to be a better choice than its dried version.
If you choose to include these options in your diet, do so with moderation and careful attention to your medications and blood sugar levels.
10 lowest-carb fruit choices for people with diabetes
When it comes to labeling a fruit as “low-carb,” it’s all relative, because fruit simply is a source of pure carbohydrates. This list includes the top 10 fruit (and berry) choices that contain the least carbs, making them the ideal options for people with diabetes.
Raspberries are one of the most seemingly elegant fruits — and they’re usually pretty expensive. They’re also remarkably low in carbohydrates after subtracting the fiber.
In fact, you might even find that a small handful doesn’t impact your blood sugar at all. 1 cup of fresh raspberries contains 15 grams of total carbohydrate and only 7 grams of net carbs!
If raspberries are a little too tangy for you, blackberries are a great alternative and equally low-carb. 1 cup of fresh blackberries also contains 15 grams of total carbohydrate and only 7 grams of net carbs.
The only downside is that blackberries tend to be one of the pricier fruits at the grocery store.
Blueberries are usually affordable and relatively low-carb.1 cup of fresh blueberries contains 21 grams of total carbohydrate and 18 grams of net carbs.
Just be careful while eating because it’s very easy to eat 2 cups of blueberries while mindlessly watching T.V. And 2 cups will definitely make themselves apparent in your blood sugar.
The great thing about strawberries is that they are very filling and relatively large compared to other berries. 1 cup of whole strawberries contains 11 grams of total carbohydrate and 8 grams of net carbs.
A few strawberries go a long way when it comes to snacking on them for a healthy dessert after dinner or slicing a few into your chia-seed pudding for extra sweetness and flavor.
Plums are small, but making a snack out of one or two is a pretty flavorful way to enjoy fruit without much impact on your blood sugar.
1 fresh plum contains about 7 grams total carbohydrate and 6.5 grams of net carbs. The only tricky part is waiting for them to ripen in your fruit basket! Plums require patience!
Tangerines (and clementines) are a good choice of citrus if you’re trying to keep the carb-count low. But do keep in mind that you’re crossing over into the world of very juicy fruits, and you will see the impact on your blood sugar.
Considering the size of a grapefruit — and the amount of time it takes to eat it — that’s a pretty satisfying snack at 18 grams of carb.
Peaches! My favorite fruit on this list, for sure. An in-season and perfectly ripe peach is a treat.
1 medium-sized peach contains 15 grams of total carbohydrate and 13 grams of net carbs. Definitely sweeter than berries, but every bite is full of wonderful texture and flavor.
When it comes to melon, you get a lot of bulk for fewer carbs compared to many other fruits.
1/8 wedge of honeydew melon contains 11 grams of total carbohydrate and 10 grams of net carbs. This means you could eat half an entire honeydew melon in one sitting (which I often did during my first pregnancy) for only about 34 grams of net carbs.
A pretty big snack for relatively few carbs.
Perhaps harder to find in the average grocery store unless you’re living on the west coast or in the deeper southern hemisphere, papaya definitely qualifies for the lower-carb list.
Are you are looking for a new healthy chicken recipe to add to your nightly meal plan? Look no further than the trim and terrific Cajun Blackened Chicken recipe from Holly Clegg’s Gulf Coast Favorites cookbook! This healthy easy recipe does not disappoint. If you are not familiar with Blackening, it refers to the cooking method of using a hot skillet to produce a slightly burnt-looking, dark-brown exterior to your food with a moist interior. It originated from Chef Paul Prudhomme’s New Orleans restaurant and blackening has since become a favorite prepared worldwide. Blackening is a quick way to keep your food moist and juicy. This blackened chicken breast recipe will be a family favorite.
Cajun Blackened Chicken
One of our family favorites! You can just make the blackened chicken breast recipe with or without the sauce.
1tablespoon chili powder
1teaspoon light brown sugar
1 1/2pounds boneless skinless chicken breasts, cut into strips
1tablespoon olive oil
1 green bell peppercored and chopped
1 red bell peppercored and chopped
1cup chopped red onion
1(5-ounce) can evaporated skim milk
1/4cup chopped green onions
In large resealable bag, combine paprika, chili powder, brown sugar, pepper, salt. Add chicken, shake to coat.
In large nonstick skillet coated with nonstick cooking spray, heat olive oil over medium heat, then sauté chicken 5–7 minutes or until browned and done. Remove to a plate.
In same skillet, add green pepper, red pepper, onion, scraping bits from bottom of pan. Cook over medium heat 5 minutes or until tender.
Add evaporated milk, stirring for one minute or until heated and bubbly. Serve chicken with sauce, sprinkle with green onions, if desired.
Blackened Chicken Breast Recipe is Diabetic-Friendly Chicken Dinner
Holly Clegg’s Gulf Coast Favorites cookbook gives you the best healthy Cajun recipes. Who doesn’t like the wonderful Cajun and Creole recipes? All your favorite healthy Louisiana recipes so you can make them at home and easily. Even this Cajun Crawfish Cakesrecipe is easy!
So, don’t fret, as Holly’s trim and terrific blackening approach will have your mouth dancing with flavor without the added fat that usually characterizes this Cajun blackened chicken recipe of amazing blends of seasoning and loads of melted butter. This cooking method is a perfect way to eat low fat, diabetic-friendly meals without missing any flavor. Because of the crispy crust of seasonings that forms when searing in the juices of a blackened dish – no added butter needed!
Do you have kitchen scissors? If not, kitchen scissorsare truly one of the best gadgets. Use them to cut poultry into tenders or to trim chicken. Wow, it makes trimming all meat and fish so easy!
When you are making the blackened chicken recipe, you can buy chicken breasts and cut into tenders yourself. They are dishwasher safe and any gadget that helps cut kitchen time is of top priority. You will find so many uses for kitchen scissors from trimming chicken to cutting pizza.
More Diabetic Cajun Recipes Like Blackened Chicken Breast Recipe
In rodents, brown adipose tissue (BAT) regulates cold- and diet-induced thermogenesis (CIT; DIT). Whether BAT recruitment is reversible and how it impacts on energy metabolism have not been investigated in humans. We examined the effects of temperature acclimation on BAT, energy balance, and substrate metabolism in a prospective crossover study of 4-month duration, consisting of four consecutive blocks of 1-month overnight temperature acclimation (24°C [month 1] → 19°C [month 2] → 24°C [month 3] → 27°C [month 4]) of five healthy men in a temperature-controlled research facility. Sequential monthly acclimation modulated BAT reversibly, boosting and suppressing its abundance and activity in mild cold and warm conditions (P < 0.05), respectively, independent of seasonal fluctuations (P < 0.01). BAT acclimation did not alter CIT but was accompanied by DIT (P < 0.05) and postprandial insulin sensitivity enhancement (P < 0.05), evident only after cold acclimation. Circulating and adipose tissue, but not skeletal muscle, expression levels of leptin and adiponectin displayed reciprocal changes concordant with cold-acclimated insulin sensitization. These results suggest regulatory links between BAT thermal plasticity and glucose metabolism in humans, opening avenues to harnessing BAT for metabolic benefits.
Unhealthy diet and physical inactivity are the major culprits to the obesity crisis, although other environmental factors may also contribute (1). An overlooked component in energy balance is adaptive thermogenesis, which comprises diet-induced thermogenesis (DIT) and cold-induced thermogenesis (CIT). DIT is the portion of energy expended after food ingestion, beyond the energy cost of digestion/absorption (2). The CIT response defends core temperature during cold exposure (3). In rodents, both processes are chiefly regulated by brown adipose tissue (BAT). Through the action of uncoupling protein 1 (UCP1), energy is converted into heat and represents a form of energy expenditure (EE) as energy is dissipated to the environment. BAT stimulation protects animals against diet-induced obesity and glucose intolerance (4).
In addition to “classic BAT” in the interscapuar region, cold exposure also induces the emergence of brown adipocyte-like cells (beige/brite adipocytes) within white adipose tissue (WAT) in animals (5,6). Brown/beige fat generates heat from glucose/lipids, and their high substrate utilization underlies protection against diet-induced insulin resistance in genetic, pharmacological, and/or transplantation models of invigorated brown/beige fat status (7–9). In humans, histological examination had demonstrated the presence of BAT in adult in the 1970–1980s (10–12), although BAT whole-body abundance was not fully appreciated until its visualization was made possible by positron emission tomography (PET)/computed tomography (CT) (13–17). BAT is not only inducible in humans (18,19) but also exhibits oxidative capacity (20) and classic BAT/beige fat features (21,22), thus forming the basis for the quest of BAT/beige fat-enhancing strategies as antiobesity treatments (23).
Acute cold exposure (hours) increases BAT activity (13,15–17,24), while longer-term exposure (days/weeks) expands BAT volume (25,26). Because BAT recruitment could reduce adiposity (26), it suggests that BAT may impact whole-body energy homeostasis. The corollary is that reduced cold exposure could suppress BAT/beige fat function in humans, with potential obesogenic consequences (27). To date, cold exposure is the best-known activator (15–17) and recruiter (25,26) of BAT, and associative data have linked higher BAT abundance with leanness and lower glycemia in humans (13,15,28,29). Whether BAT withers under warm exposure and whether BAT recruitment triggers compensatory metabolic and/or behavioral adaptations have not been investigated but are integral to BAT physiology. Rodent studies have revealed a complex interplay between housing temperature, BAT recruitment, and energy balance, which ultimately determines metabolic phenotype (30). For better appreciation of the metabolic significance of human BAT and the implications of BAT status on health, BAT recruitment interventions should be examined in the context of whole-body energy metabolism.
In this study, we investigated the effects of long-term mild cold and warm exposure by minimal overnight manipulation of ambient temperature on individual BAT status and the corresponding energy/substrate homeostatic responses. We hypothesized that human BAT exhibits plasticity and its activity modulates systemic energy metabolism.
Research Design and Methods
Five healthy men were recruited through local advertisement and provided written informed consent. The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)–National Institute of Arthritis and Musculoskeletal and Skin Diseases Institutional Review Board approved the study: Impact of Chronic Cold Exposure in Humans (ICEMAN). Supplementary Fig. 1 summarizes recruitment, allocation, and intervention.
This is a prospective crossover study consisting of four consecutive blocks of 1-month duration (Supplementary Fig. 2): it incorporates 1) sequential monthly thermal acclimation over 4 months and 2) acute thermometabolic evaluations at the end of each study temperature regimen. Volunteers were admitted to the Clinical Research Unit (NIDDK) in Bethesda, MD, (April–November 2013) for the entire 4 months.
Monthly Thermal Acclimation
Volunteers resided in a temperature-adjusted private room, engaged in usual daily activities, and returned to their room each evening. Room temperature was adjusted in the following sequence: 24°C (month 1) → 19°C (month 2) → 24°C (month 3) → 27°C (month 4). Volunteers were exposed to the study temperature for at least 10 h each night, wearing standardized hospital clothing with a combined thermal insulation value of 0.4 (clo). Only bedsheets were provided. Volunteers were asked to not deviate daily activity level over the study period. Each subject therefore acted as his own control. At 0800 h at the end of each month, volunteers were admitted to a whole-room indirect calorimeter for thermometabolic evaluation.
Volunteers wore two temperature data loggers (cat. no. RHT20; Extech, Nashua, NH): one “external to clothing” to track environmental temperature and the other “within clothing” to track immediate temperature changes in the “microenvironment” within clothing. We averaged individual exposed temperature every 30 min for the entire 4-month period, allowing us to record environmental temperature variations and the “true temperatures” the individual was being exposed to.
All meals, including prepacked lunches/snacks, were provided with the following composition: 50% carbohydrate, 20% protein, and 30% fat. The first month was an equilibration period, during which volunteers followed a weight-maintenance diet. After month 1, subjects ate according to hunger. Caloric/macronutrient content was calculated based on weight-maintenance requirements, determined during equilibration month. Any unconsumed foods were returned/weighed for energy/macronutrient intake calculation. Subjects met study dietitians twice weekly to verify food diaries/compliance. Total intake/macronutrient was computed/analyzed using three-dimensional food models (ProNutra, version 184.108.40.206.; Viocare Technologies, Princeton, NJ).
Subjects completed questionnaires assessing appetite twice a week before/after breakfast by marking on a visual analog scale (VAS) (10 cm long) responses to the following questions: 1) How hungry are you? 2) How full are you? 3) How much food can you consume? These questions gauged hunger, satiety, and desire to eat before/after meals.
Before each monthly thermaometabolic evaluation, volunteers underwent an ad libitum meal test, consisting of a selection of food items displayed in a vending machine. Subjects ate until they felt “comfortably full.” Total energy/macronutrient intake were recorded, together with ratings of appetite (hunger, satiety, and desire to eat) using the same weekly questionnaire at T = −10, 0, 60, 120, 180, 240, and 300 min where initiation of the meal was defined as T = 0 min.
Acute Thermometabolic Evaluations
Thermometabolic evaluation was scheduled at the end of each month (Supplementary Fig. 2), modeled on our previous published methods (24,31), with total EE calculated as previously described (24,31). Volunteers underwent two 24-h sessions in a whole-room calorimeter, exposed to first 24°C (day 1) and then 19°C (day 3), with a resting 24-h period in between. The temperature order was not randomized because our previous study did not reveal a sequence effect (31). Testing at the two temperatures allowed us to evaluate how monthly acclimation modulated EE/metabolism at both thermoneutral and mild cold conditions. Lunch (Boost Plus; Nestlé Healthcare Nutrition, Inc., Vevey, Switzerland) and dinner (selected from Metabolic Menu) were provided at 1300 and 1900 h, consisting of one-third and two-thirds of daily caloric intake, respectively, based on calculation from equilibration month. CIT was calculated as difference in total EE between 24°C and 19°C and DIT as difference in pre- (0800–1300 h) and post- (1300–1900 h) lunch EE. As the test meal carried identical caloric and macronutrient content, we attributed any changes observed to arise from adaptive thermogenesis because the facultative component (i.e., digestion/absorption) should be relatively unaltered. Shivering response was quantified by surface electromyography (EMG), as previously described (32), and volunteers reported perception to cold each month during EE testing using VAS. Hormonal/metabolic parameters were measured in venous samples. Postprandial insulin sensitivity was calculated after a mixed meal (33) and adipose resistance index as the product of free fatty acid × insulin. At the conclusion of the thermometabolic study, body composition was measured, as previously published (24,31).
PET/CT was performed using Siemens Biograph mCT (Siemens Healthcare) (32). PET/CT was undertaken at 0800 h the morning after the 19°C testing day at the end of each acclimation month. Attenuation-corrected PET/CT images were analyzed using custom software built with IDL (Exelis Visual Information Solutions, Inc., Boulder, CO). A three-dimensional region of interest (ROI) was defined cranially by a horizontal line parallel to the base of the C4 vertebra and caudally by an oblique line traversing the manubriosternal joint and T8 transverse process (Supplementary Fig. 3). BAT was defined as tissue with Hounsfield units (HU) −300 to −10 on CT (i.e., fat density) with a lean body mass standardized uptake value (SUV) of ≥2 (i.e., high glucose uptake). The chosen ROI captures major BAT depots in the cervical, supraclavicular, axillary, superior mediastinal, and paravertebral areas. This ROI was chosen because spurious myocardial/renal excretory fluorodeoxyglucose (FDG) uptake could not be reliably excluded from BAT. This approach allowed examination of BAT evolution within a well-defined region of adipose tissue across 4 months.
The following parameters were analyzed: BAT volume, mean SUV, and activity. BAT volume, defined as the sum of the volume of all voxels that met HU-SUV criteria, represents activated BAT. Mean SUV (normalized by FDG dose and lean body mass) of ROI represents mean metabolic activity within BAT-harboring region. BAT activity represents the total radioactivity (in MBq) within ROI and captures both changes in volume and mean FDG uptake. Furthermore, because fat exhibits metabolic activity as a continuum and the chosen SUV threshold of ≥2 is arbitrary and may potentially exclude more diffuse enhancement of adipose metabolic activity, we also quantified mean SUV in the entire ROI within tissue of fat density (HU: −300 to −10). Mean SUV of whole fat depot estimates overall metabolic activity and may capture both BAT and diffuse beige fat activity. This is particularly relevant in subjects with lower BAT abundance (Supplementary Figs. 5 and 7). While BAT, defined with an SUV threshold of ≥2, was not visually apparent in these two subjects, whole fat activity followed the same pattern of acclimated BAT changes. When a lower SUV was used (≥1) (Supplementary Fig. 8), adipose activity changes were visually concordant with overall fat activity. Mean SUV uptake in liver and skeletal muscle (rectus femoris) was quantified to compare temperature-acclimation impact on BAT and other metabolic organs. All images were analyzed twice by an investigator (P.L.) blinded to subject identity and acclimation temperature. Intrascan coefficient of variation of BAT volume, mean SUV, BAT activity, and mean whole fat activity were 0.7%, 3.0%, 1.3%, and 2.4%, respectively.
Paired subcutaneous adipose/muscle biopsies were obtained at the end of each month from abdomen and rectus femoris, respectively (31). RNA extraction and cDNA synthesis were performed using standard methods, and genes governing thermogenesis and glucose metabolism were examined using TaqMan Gene Expression assays (Applied Biosystems) (Supplementary Table 2).
Plasma adiponectin, leptin, and fibroblast growth factor 21 (FGF21) were measured by ELISA (R&D Systems, Minneapolis, MN, and BioVendor, Oxford, U.K.), according to manufacturer’s protocol, with intra-assay/interassay coefficients of variation between 2.5 and 4.8%. Remaining tests were measured by the Department of Laboratory Medicine, National Institutes of Health (NIH).
Statistical analysis was performed using SPSS 20.0 (SPSS, Inc., Chicago, IL). Data are expressed as means ± SD. Trend changes of physiologic and hormonal parameters during temperature acclimation across 4 months, expressed as fold change over baseline, were analyzed by one-way ANOVA with Bonferroni correction. Areas under the curve (AUCs) were calculated using the trapezoidal rules incorporating sampling points across a 24-h period from 0800 to 0700 h the next morning (Supplementary Fig. 2). Postprandial glucose and insulin AUCs were calculated in the period after lunch starting at 1300 h (T = 0, 60, 120, 240, and 360 min). Pearson correlation coefficients were used to examine associations between variables. An α-error of 0.05 was considered statistically significant.
Baseline Acute Thermometabolic Evaluation
Five men (21 ± 2 years old, BMI 22 ± 1 kg/m2, body fat 21 ± 2%) participated in the study. Volunteers were first evaluated at baseline for BAT status and thermometabolic responses to temperature changes. Compared with 24°C, mild cold exposure at 19°C increased total EE by 6 ± 4% (P < 0.05), representing CIT response. Baseline cold-activated BAT volume was 55 ± 61 mL, with a mean SUV of 3.2 ± 0.8. EE at 19°C correlated positively with BAT volume (R2 = 0.82, P = 0.03). These results replicated findings in our previous overnight cold exposure studies (24,31) and validated the methodology in the investigation of temperature acclimation–associated metabolic and physiologic consequences. Hereafter, we describe changes in physiologic and metabolic parameters at each monthly thermometabolic evaluation, with results stratified to either the 19°C or the 24°C testing condition to decipher impact of acclimation on metabolism under thermoneutrality and mild cold exposure.
Metabolic Consequences of Monthly Acclimation
Tables 1–4 summarize changes in BAT and physiologic, dietary, body compositional, and hormonal parameters across the 4-month acclimation. Hormone/metabolite AUC results are shown in Table 4 and fasting levels in Supplementary Table 3. Results from each domain are described in the following subsections.
PET/CT parameters across 4 months of acclimation
Physiologic parameters across 4 months of acclimation
Nutritional and body compositional parameters across 4 months of acclimation
Hormonal and metabolic parameters across 4 months of acclimation
Figure 1A–D demonstrates BAT evolution in one representative subject throughout the 4-month sequential acclimation. Supplementary Figs. 4–7 show individual results. Figure 1E–H displays mean changes in BAT volume and overall fat metabolic activity, which increased upon cold acclimation (19°C) by 42 ± 18% (P < 0.05) and 10 ± 11% (P < 0.05), respectively; decreased after the thermoneutral month (24°C) to nearly baseline level; and completely muted at the end of the 1-month warm exposure period (27°C). BAT radiodensity, measured in HU, responded to acclimation with the same pattern (P < 0.01) (Table 1). BAT HUs increased by 25 ± 8% after cold acclimation, reversed after the thermoneutral month, and by the end of warm acclimation in month 4, HU was 18 ± 11% lower than baseline values in month 1 (Table 1). In contrast, mean SUV of skeletal muscle and liver remained unchanged during acclimation (Table 1). Room (P < 0.05) and individually exposed temperatures (P < 0.01), but not outdoor temperatures, correlated with BAT changes during the study period (Fig. 1I and J and Supplementary Table 1).
Temperature-dependent BAT acclimation. A–D: Representative PET/CT fused images of the cervical-supraclavicular region (left panels: coronal view; right panels: transverse view) of one subject during monthly temperature acclimation. BAT (HU: −300 to −10 and SUV ≥2) is shown in red. Baseline BAT volume and mean SUV and activity were 26 mL and 2.65 and 0.238 MBq, respectively (A). All BAT parameters increased after 1 month of mild cold acclimation (19°C) (B), decreased to nearly baseline level after the thermoneutral month (24°C) (C), and BAT was nearly completely muted at the end of the 1-month mild warm exposure in the final month (27°C) (D). Mean fold changes (N = 5) of BAT volume (E) and mean SUV (F) and BAT activity (G), relative to month 1 (24°C), were significant across 4-month acclimation. Whole fat activity, as defined by 18F-fluodeoxyglucose uptake within tissue of fat density (HU: −300 to −10), followed the same pattern (H) and interacted significantly with temperature acclimation. Room (I) and individual exposed temperatures (J), but not environmental seasonal fluctuations (I), tracked BAT and whole fat metabolic changes in the predicted temperature-dependent manner. Correlative analysis between BAT parameters and temperature exposure is shown in Supplementary Table 1. Individual PET/CT images and temperature profiles are shown in Supplementary Figs. 4–7. *P < 0.05 compared with month 1 (24°C); #P < 0.05 compared with month 2 (19°C).
Cold- and Diet-Induced Thermogenesis
We next explored metabolic consequences of BAT acclimation. CIT response did not change significantly during temperature acclimation (Table 2). In contrast, DIT measured at 19°C rose by 32 ± 35% (P = 0.03) after cold acclimation. Progressive rewarming suppressed 19°C DIT response at months 3 and 4 to nearly baseline level. DIT measured at 24°C was unaltered (Table 2).
Shivering Response and Cold Sensitivity
Surface EMG recordings of muscle fasciculation/shivering measured at 19°C and 24°C were not different (Table 2), indicating absence of significant shivering and validating our model in capturing nonshivering thermogenesis. Monthly acclimation did not alter EMG recordings, and subjects did not report changes in cold perception at 19°C during monthly calorimeter testing (Supplementary Fig. 9).
Diet and Body Composition
Neither total caloric nor macronutrient content of intake changed during acclimation (Table 3). Biweekly hunger and satiety scores did not change significantly (Table 3); however, volunteers reported an increase in desire to eat and reduction in satiety during ad libitum meal test after cold acclimation, which reversed during the warm months (Supplementary Fig. 10). Body composition was unaltered across the study period (Table 3).
To elucidate potential endocrine mediators of BAT acclimation, we profiled pituitary-thyroid-adrenal axes (Table 4). Cold acclimation increased free triiodothyronine (T3) AUC measured at 24°C but not at 19°C. Free T3 to free thyroxine (T4) ratio (an indicator of peripheral T4 to T3 conversion ) was greater by 11 ± 5% (P = 0.01), measured at 24°C. No significant changes were observed in thyrotropin (thyroid-stimulating hormone [TSH]) or the pituitary-adrenal axis.
Total glucose and insulin AUCs did not change during acclimation (Table 4). In contrast, postprandial insulin excursion measured at 19°C reached a nadir after cold acclimation, without significant changes to glucose excursion (Fig. 2A and B). Indices of insulin sensitivity and resistance showed significant reciprocal changes during cold and warm acclimation, consistent with an improvement of postprandial whole-body insulin sensitivity after cold acclimation (Fig. 2C and D). These changes were absent during measurements at 24°C (Fig. 3A–D).
Metabolic consequences of BAT acclimation at 19°C. A and B: Comparison of postprandial glucose and insulin excursions after a mixed meal at 1300 h before and after cold acclimation, respectively, measured at 19°C. Glucose excursions were unchanged but insulin levels decreased, with a significant reduction in AUC, after mild cold acclimation (month 2). Accordingly, adipocyte insulin resistance (IR) was the lowest (C) and Matsuda index (an indicator of insulin sensitivity) was the highest (D) after cold acclimation (month 2). These changes in glucose metabolism were accompanied by an increase in circulating adiponectin (E) and a decrease in circulating leptin (F). Cold acclimation–induced changes (months 1 and 2) in circulating adiponectin (G) and leptin levels (H) correlated negatively with changes in BAT activity. Adiponectin and leptin mRNA displayed concordant changes in subcutaneous adipose tissue biopsies with circulating levels, and changes in GLUT4 tracked those of adiponectin (I). aP < 0.05 compared with month 1 (24°C), bP < 0.05 compared with month 2 (19°C), cP < 0.05 compared with month 3 (24°C), and dP < 0.05 compared with month 4 (27°C).
Metabolic consequences of BAT acclimatization at 24°C. A and B: Comparison of postprandial glucose and insulin excursions after a mixed meal at 1300 h before and after cold acclimatization, respectively, measured at 24°C. Unlike measurements at 19°C (Fig. 2A and B), no significant changes were observed in glucose or insulin excursions. Accordingly, adipocyte insulin resistance (IR) (C) and Matsuda index (an indicator of insulin sensitivity) (D) were unchanged. Circulating adiponectin increased (E), while leptin decreased (F), identical to measurements observed at 19°C (Fig. 2E and F). Cold acclimatization–induced changes (months 1 and 2) in circulating adiponectin (G) and leptin levels (H) correlated negatively with changes in BAT activity. In contrast to that observed in adipose tissue (Fig. 2I), adiponectin and GLUT4 mRNA did not change significantly in muscle (I). cP < 0.05 compared with month 3 (24°C); dP < 0.05 compared with month 4 (27°C).
Given our recent demonstration of BAT as an endocrine organ in humans (19,32,35), we probed adipokine changes during acclimation. Adiponectin AUC was augmented by 22 ± 9% (P < 0.001) after cold acclimation (Fig. 2E). Not only was enhancement of adiponectin levels observed at 19°C during acute thermometabolic evaluation, but similar increase also occurred at 24°C (P < 0.001) (Fig. 3E). In contrast, cold acclimation reduced leptin AUC by 14 ± 28% (P < 0.001), evident at both 19°C (Fig. 2F) and 24°C (Fig. 3F). These dichotomized changes returned almost to baseline during the thermoneutral third month, trending to the opposite directions at the end of the fourth month at 27°C (P < 0.05). Changes in circulating adiponectin and leptin correlated negatively with changes in BAT activity after cold acclimation (Fig. 2G and H and Fig. 3G and H). FGF21 AUC rose after cold acclimation, although overall trend did not reach significance (Table 4).
Fat and Muscle Gene Expression
For exploration of sources of adipokine and origins of metabolic changes, fat and muscle biopsies were obtained from four volunteers at the end of each month. Adiponectin and GLUT4 expression in adipose tissue (Fig. 2I), but not muscle (Fig. 3I), rose after cold acclimation, while expression of leptin fell, and their respective trends reversed after thermoneutral and warm acclimation months (P < 0.05). Expression of CIDEA, a BAT gene governing lipid mobilization (36), increased after cold acclimation but decreased during rewarming (Fig. 4). No other BAT/beige fat gene changes were observed.
BAT and beige fat gene changes in adipose tissue biopsies across 4-month acclimatization. A: Changes in general BAT gene expression (general BAT genes are defined as genes ascribed to general BAT function and do not indicate their developmental origin). Expression of CIDEA, but not others, changed significantly (P = 0.04) during acclimatization across 4-month period. B: Changes in classic BAT gene expression. Classic BAT genes are defined as those expressed in interscapular BAT in animals or human infants (50). C: Changes in beige fat gene expression. Beige fat genes are defined as those expressed in inducible brown adipocytes, also known as brite or beige adipocytes, found within WAT depots. No significant changes were observed in classic BAT or beige fat genes across temperature acclimation.
The major finding of our study is the demonstration of BAT acclimation and its metabolic consequences by minimal manipulation of overnight temperature exposure while allowing usual daily activities. Human BAT is inducible and suppressible by controlled mild cold and warm exposure, respectively, independent of seasonal fluctuations. BAT acclimation is accompanied by boosting of DIT and postprandial insulin sensitivity. Mechanistically, this is associated with reciprocal changes of circulating adiponectin and leptin, mirrored by corresponding transcriptosomal changes in adipose tissue ex vivo. These results provide the first evidence linking ambient temperature, BAT acclimation, and whole-body energy/substrate metabolism in humans.
Consistent with previous reports (25,26), we confirmed BAT recruitability by cold exposure but did not observe significant CIT response augmentation; the latter could be a type 2 error. Despite tentalizing associative data linking BAT abundance with favorable energy metabolism in humans, it remains unclear, to date, whether BAT recruitment is accompanied by metabolic benefits. We specifically sought to determine the significance of BAT recruitment and revealed an association of BAT acclimation with enhancement of postprandial energy metabolism and insulin sensitization. Within the allowance and feasibility of human research, we explored underlying mechanisms through blood and tissue analyses.
First, within the pituitary-thyroid-adrenal axis, we observed an increase in T3-to-T4 ratio, which indicates enhanced T3 synthesis. Given the enrichment of BAT with type 2 deiodinase (37) and our previous report showing severe insulin resistance amelioration by thyroid hormone-mediated BAT activation (38), we hypothesize heightened T3 synthesis within BAT to be one plausible mechanism underlying acclimated-BAT associated metabolic changes. Such a pattern of increased thyroid hormone turnover in the absence of TSH changes is reminiscent of cold adaptation observed among Arctic residents (39).
Second, our adipokine profiling uncovered an intriguing relation between BAT, adiponectin, and leptin. Cold acclimation augmented circulating adiponectin but decreased leptin. It is tempting to speculate that cold-induced adiponectin, a potent insulin sensitizer, contributes to glucose metabolism improvement and leptin reduction, with the latter as a result of improved tissue sensitivity. Concordant gene changes in adipose adiponectin and leptin, absent in muscle, argue adipose to be the primary effector. Surprisingly, circulating adiponectin related negatively with BAT activity, suggesting that PET-detectable BAT was not the source of cold-induced adiponectin. As BAT exhibits insulin-independent glucose uptake capacity (40), lesser BAT expansion could have triggered alternative glucose utilizing pathways in WAT during cold acclimation, evident by observed WAT GLUT4 upregulation. Interestingly, such changes in circulating adiponectin and leptin were not limited to the cold-exposed condition (Fig. 2) but persisted at thermoneutrality (Fig. 3), indicating that the temperature-acclimated hormonal milieu was not totally dependent on BAT activation. The corollary is that acclimated BAT could be serving beneficial metabolic functions not related to temperature regulation per se.
Third, newly identified cytokines, such as FGF21, may mediate temperature-acclimated tissue cross-talk. Recent identification of a FGF21-adiponectin feed-forward axis (41) led us to wonder whether FGF21 augmentation after cold acclimation could have brought forth the adiponectin rise. When BAT was muted at the end of warm acclimation and adiponectin dwindled, FGF21 did not fall, suggesting that non-BAT FGF-secreting tissues might have compensated in states of relative BAT deficiency.
Fourth, although we did not observe an increase in beige fat gene expression, possibly due to the small sample size, we speculate fat browning to be a possibility. This is corroborated by finding an increased expression of the BAT gene CIDEA in adipose tissue after cold acclimation. Although ethics considerations prohibited serial neck fat biopsies in our volunteers, changes in radiodensity within BAT by PET/CT have offered insight on tissue changes. Adipose tissue is typically characterized by HU between −10 and −300, in contrast to muscle tissue, whose HU is within the positive range. Compared with WAT, BAT has relatively less lipid, as it is filled with abundant mitochondria and blood vessels. This is exemplified by water-fat separated magnetic resonance imaging revealing a lower fat fraction in activated BAT both in humans (42) and in rodents (43). We speculate that the rise and fall in BAT radiodensity with cold and warm acclimation, respectively, could be reflections of WAT → BAT transformation (or fat browning). This is also supported by previous studies demonstrating cell-autonomous (44) and endocrine-mediated (19) cold-induced WAT browning in humans. Further studies are required to ascertain whether WAT browning contributes to cold-acclimated BAT-induced metabolic changes.
Collectively, our results infer a complex concerted BAT-WAT response to cold acclimation, which could involve interplay between CIDEA-mediated lipid mobilization (45,46), GLUT4-enhanced glucose utilization, and FGF21/adiponectin-induced insulin sensitization. Most importantly, all these changes occurred in the absence of measureable EE, caloric intake, or body compositional alterations, suggesting such responses to be primary cold-induced metabolic sequelae rather than compensatory physiologic adaptations. Nonetheless, because the desire to eat heightened after cold acclimation, we cannot exclude the possibility that appetite stimulation could diminish metabolic benefits of BAT recruitment if it increases caloric intake in longer-term studies.
The inducibility, suppressibility, and plasticity of human BAT entail implications beyond thermoregulatory physiology. The translation of recently discovered BAT activators in the laboratory to pharmacologic BAT stimulants available for clinical use is not a trivial process (23). Our study substantiates, in contrast, a simple BAT-modulating strategy: a mild reduction in environmental temperature is capable of recruiting BAT and yielding associated metabolic benefits; conversely, even a small elevation in ambient temperature could impair BAT and dampen previously attained metabolic benefits. Such reversible metabolic switching, occurring within a temperature range achievable in climate-controlled buildings, therefore carries therapeutic implications of BAT acclimation both on an individual and a public health level. Bedroom temperature has gradually increased from 19°C to 21.5°C over the last three decades in the U.S. (47). The blunting of BAT function due to widespread use of indoor climate control could be a neglected contribution to the obesity epidemic. Moderate downward adjustment of indoor temperature could represent a simple and plausible strategy in dampening the escalation of obesity on a population level. Our volunteers reported satisfactory sleep during acclimation, although more formal assessment of sleep quality is required in future studies.
Our findings should be viewed as a proof of concept illustrating human BAT plasticity. We acknowledge the small sample size to be a limitation of our study. Unfortunately, the conduct of long-term acclimation study necessitated substantial resources and regrettably prohibited a large sample size. Despite a small study population, the investigations were undertaken in a tightly monitored and controlled yet real-life simulating and applicable setting encompassing the most comprehensive spectrum of energy balance/metabolism to date to tackle a question fundamental to human BAT research: What is the significance of BAT recruitment? The unveiled positive relation between acclimated BAT and glucose homeostasis is clinically relevant. Glucose intolerance is an independent risk factor of cardiovascular mortality, and postprandial hyperglycemia is its earliest manifestation (48). We emphasize that a causal linkage could not be definitely ascertained between BAT recruitment and postprandial insulin sensitivity improvement; however, our study provides compelling circumstantial evidence supporting a potential therapeutic role of BAT in impaired glucose metabolism and calls for the investigation of similar temperature acclimation in individuals with impaired glycemia. Our observation of BAT recruitment accompanied by insulin sensitization in the absence of significant weight loss echoes animal findings showing glucose homeostasis improvement after fat browning to be greater than expected from adiposity reduction alone (49,50). Whether it was indeed a result of fat phenotypic and/or adipokine changes merits further studies.
In summary, temperature acclimation modulates BAT abundance and activity, subsequently impacting energy and substrate metabolism in humans. BAT exhibits thermal plasticity intimately related to glucose homeostasis. Harnessing BAT by simple adjustment of ambient temperature could be a new strategy in the combat against obesity, diabetes, and related disorders.
Acknowledgments. The authors thank Dr. Peter Herscovitch and Dr. Corina Millo, both from the PET Department, Clinical Center, NIH, for advice on PET/CT scanning; Rachel Perron, Christopher Idelson, Sarah Smyth, Jacob Hattenbach, and Juan Wang, all from Diabetes, Endocrinology, and Obesity Branch, NIDDK, NIH, for technical assistance; Dilalat Bello and Oretha Potts, from the Clinical Center, NIH, for dietary counseling/monitoring; and all nurses in the Clinical Metabolic Unit, NIH, for their nursing care.
Funding. This study was supported by the Intramural Research Program Z01-DK047057-07 of NIDDK and the NIH Clinical Center. P.L. was supported by an Australian National Health and Medical Research Council Early Career Fellowship, the Diabetes Australia Fellowship and Bushell Travelling Fellowship, and the School of Medicine, University of Queensland.
The funders had no role in the design or conduct of the study; collection, management, analysis, or interpretation of data; or preparation, review, or approval of the manuscript.
Duality of Interest. No potential conflicts of interest relevant to this article were reported.
Author Contributions. P.L. participated in the development of the study concept and design, research, acquisition of data, and analysis and discussion of results; wrote the manuscript; participated in critical revision; and approved the final version of the manuscript. S.S., J.L., A.B.C., R.J.B., K.Y.C., and F.S.C. participated in the development of the study concept and design, research, acquisition of data and analysis and discussion of results; participated in critical revision; and approved the final version of the manuscript. W.D. and C.D.W. researched and analyzed data, contributed to discussion of results, participated in critical revision, and approved the final version of the manuscript. P.L. and F.S.C. are the guarantors of this work and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.
Prior Presentation. Parts of this study were presented in abstract form at ICE/ENDO 2014, Chicago, IL, 22 June 2014.
This oven-roasted tomato sauce is bursting with flavor but still wonderfully light! It’s so delicious, you’ll be amazed how simple it is to make.
It’s hard to find a decent tomato sauce at the store. Many are full of sugar, high in sodium, and contain unnecessary fillers and preservatives.
The solution? Make this oven-roasted tomato sauce right at home! You’ll be amazed how simple it is to prep, and the flavor is so much better than anything you could get from the store.
If you’ve never tried roasting your tomatoes, you’re in for a treat. Roasting them intensifies their taste, which means your sauce will have a rich, complex flavor you just can’t get from cooking it on the stove!
Roasting the tomatoes may take a bit of time, but the process itself is quite simple. And once your sauce is made, you can store it in the freezer to enjoy for months!
How to make oven-roasted tomato sauce
Ready to see how easy it is to make this wonderful sauce right in your own kitchen?
Step 1: Preheat the oven to 450°F.
Step 2: In a large bowl, combine the quartered tomatoes, chopped onion, whole garlic cloves, salt, red pepper flakes, and sugar.
Step 3: Add the olive oil and toss until the tomatoes are well-coated.
Step 4: Transfer to a 13- × 9-inch baking dish.
Step 5: Roast until the tomatoes soften, about 45-60 minutes.
Step 6: Remove the pan from the oven and allow to cool slightly.
Step 7: Drain off any excess liquid.
Step 8: For a chunkier sauce, mash the tomatoes with a potato masher right in the pan. For a smoother sauce, transfer to a food processor and process for a few seconds.
Step 9: Stir in the fresh basil and oregano.
Your sauce is ready to serve!
What to eat with this sauce
Now that you’ve made a delicious tomato sauce, what recipes should you use it in?
Of course, it will be wonderful with any classic Italian dish. Use it as the base on a cauliflower pizza crust or a sauce for your pasta. To lower the carbs, use zoodles or low-carb pasta.
For an easy and healthy chicken Parmesan, spread it over your chicken breast before baking. Once the chicken is almost done, spread the Parmesan on top to get it nice and melted. Finish with fresh basil before serving.
You can also use it in homemade chili, tomato soup, or even an enchilada sauce. The possibilities are endless!
Any extra sauce can be stored in an airtight container in the refrigerator for up to a week. I recommend using a jar with a screw top lid so it’s easy to grab some when you need it.
You can also freeze your sauce for longer storage. I suggest dividing the sauce into individual batches so it’s easy to thaw only as much as you need at a time.
Other easy tomato dishes
When tomatoes are in season, I find myself picking up a few every time I go to the store. They’re hard to resist!
Thankfully, there are so many delicious ways to cook with tomatoes. Some of my recipes call for canned tomatoes, but in the summer, I swap them out for fresh! Here are a few of my favorite recipes:
When you’ve tried this sauce, please don’t forget to let me know how you liked it and rate the recipe in the comments below!
Oven-Roasted Tomato Sauce
This oven-roasted tomato sauce is bursting with flavor but still wonderfully light! It’s so delicious, you’ll be amazed how simple it is to make.
Preheat the oven to 450°F.
In a large bowl, combine the quartered tomatoes, chopped onion, whole garlic cloves, salt, red pepper flakes, and sugar.
Add the olive oil and toss until the tomatoes are well-coated.
Transfer to a 13- × 9-inch baking dish.
Roast until the tomatoes soften, about 45-60 minutes.
Remove the pan from the oven and allow to cool slightly.
Drain off any excess liquid.
For a chunkier sauce, mash the tomatoes with a potato masher right in the pan. For a smoother sauce, transfer to a food processor and process for a few seconds.
Stir in the fresh basil and oregano.
This recipe is for 10 servings. Each serving is 1 cup of sauce. Sauce can be stored in an airtight container in the fridge. I recommend a jar with a screw top lid for convenience. You can also freeze the sauce for longer storage.
Nutrition Info Per Serving
Oven-Roasted Tomato Sauce
Amount Per Serving (1 cup)
Calories 147 Calories from Fat 103
% Daily Value*
Saturated Fat 1.6g10%
Trans Fat 0g
Polyunsaturated Fat 1.5g
Monounsaturated Fat 8g
Vitamin A 0IU0%
Vitamin C 0mg0%
Net carbs 7.5g
* Percent Daily Values are based on a 2000 calorie diet.
Course: Sauces & Condiments
Keyword: easy pasta recipes, homemade pasta sauce, tomato sauce
How often do you find yourself sweating excessively without any clear reason?
Excessive sweating as a person with diabetes isn’t a common topic of discussion, but you’re definitely not the only one dealing with it.
There are actually a number of reasons diabetes may be causing that extra sweating.
In this article, we’ll discuss different aspects of diabetes that can lead to excessive sweating and what you can do about it.
Causes of excessive sweating in people with diabetes
There are numerous reasons diabetes can cause illogical and obnoxious sweating in a person with diabetes. Some of those reasons are simple and resolved quickly, and others are far more complicated.
Let’s take a look.
Low blood sugar (hypoglycemia)
By far the most obvious and most common reason for a sudden bout of sweating, low blood sugar is one of the tedious challenges that come with managing your blood sugar levels.
Generally the result of an imbalance of insulin versus food or activity, low blood sugars can also result from a few types of non-insulin diabetes medications used to treat diabetes.
The sweating that comes with low blood sugar is the result of adrenaline. When your blood sugar is dropping, your body releases adrenaline to compensate.
Symptoms of low blood sugar (hypoglycemia) can include:
Being nervous or anxious
Sweating, chills, and clamminess
Irritability or impatience
Feeling lightheaded or dizzy
Color draining from the skin (pallor)
Feeling weak or having no energy
Tingling or numbness in the lips, tongue, or cheeks
Coordination problems, clumsiness
Nightmares or crying out during sleep
If caught early, some low blood sugars simply leave you feeling hot and on the verge of sweating. The more severe the low is, and the greater length of time your blood sugar is low, the more you will sweat.
Severe low blood sugars while you’re sleeping, for example, could persist gradually for an hour before your body wakes up and you find yourself soaked in sweat.
For some people with diabetes, sweating may be one of the first symptoms you feel when your blood sugar is dropping. For others, it may come long after lightheadedness, trembling, hunger, irritability, and tiredness.
Treatment: While the occasional low blood sugar is expected in anyone taking insulin or some non-insulin diabetes medications, frequent low blood sugars mean the dosage of your medication needs to be adjusted.
Our insulin needs change throughout our lives based on variables like your weight, age, activity level, nutrition habits, and stress level.
For example, if you start walking every day after dinner, your medication dosages will likely need an adjustment to prevent low blood sugars because your body is burning more of the glucose in your bloodstream on its own during exercise.
In general, anyone taking insulin or other medications that lower blood sugar should keep fast-acting carbohydrates nearby at all times in order to treat lows quickly and safely.
If hypoglycemia is a frequent problem and concern for you, ask your healthcare team about using a continuous glucose monitor (CGM) to help you prevent and manage your low blood sugars sooner so they don’t become as severe.
Thyroid conditions are relatively common in people with diabetes, but there are two types and only one is likely to cause excessive sweating.
Hyperthyroidism: A common consequence of persistently high blood sugar levels, hyperthyroidism is characterized by an over-active thyroid producing too much hormone.
This type of thyroid disorder is more commonly seen in people with type 2 diabetes. There is a version of hyperthyroidism that is an autoimmune condition, known as Grave’s Disease.
This type of neuropathy can develop when persistently high blood sugar levels begin to interfere with your nervous system’s ability to manage normal involuntary functions like bladder control, heart rate, and sweating.
More difficult to detect, one of the most obvious external signs of autonomic neuropathy is severely dry, cracked feet along with excessive sweating.
Treatment: The best treatment for this condition is to get your blood sugars back into a healthier range as quickly as possible. Talk to your healthcare team about medications to help manage your symptoms.
Heart failure, heart attack, or stroke
Excessive sweating can be a clear and emergent sign of heart failure, heart attack, or a stroke. If your sweating is an issue you’ve been dealing with on a regular basis for weeks and months, it’s likely not related to one of these life-threatening heart conditions.
Treatment: If you’re also experiencing symptoms of shaking, chills, and fever, you should get to an emergency room immediately. As with everything else, getting your blood sugars into a healthier range can significantly reduce your chances of developing a cardiovascular condition.
Chronic kidney disease (CKD) is a very common complication of persistently high blood sugar levels in people with diabetes.
CKD is defined by your kidney’s increasing struggle to excrete excess fluid and waste from your body. The accumulation of that fluid and waste is what usually leads to symptoms including:
Low blood pressure
Nausea, vomiting, loss of appetite
Feeling out of breath frequently
Sweating can also result from certain medications used to treat kidney disease.
Treatment: There are 5 stages of kidney disease, and the most important thing anyone with diabetes can do to prevent or manage CKD is to get your blood sugars back into a healthier range and discuss the necessary treatment steps with your healthcare team.
Obesity has been established as the leading risk factor for type 2 diabetes. Excessive sweating is a well-established symptom and complication of obesity.
In the body of an obese person, explains The Weight of the Nation, the amount of body surface area (BSA) is very low in relation to their overall weight. This means the body has more trouble eliminating body heat as quickly and easily. Sweating is the body’s next method of releasing and managing body heat.
Treatment: Losing weight is the number one most important thing you could focus on as a patient struggling with obesity. But you don’t have to go at it alone. Talk to your healthcare team! There may be certain medications, coaching, and other support available to help your pursuit of weight loss more sustainable and successful!
Overall, it’s important to note that excessive sweating may seem harmless but it’s often the sign of something far more significant.
If you’re struggling with excessive sweating, don’t dismiss it or ignore it. Contact your healthcare team in order to be sure your body isn’t dealing with something potentially dangerous that needs to be treated.
Easy Crock Pot Pork Recipes Featured in Crock Pot Convenience Chapter
Easy crock pot pork recipes make wonderful easy healthy dinner and great for eating healthy. This healthy easy recipes is one of the most delicious diabetic pork recipes. You can cook an entire meal from entree to dessert in a crock pot. Holly Clegg’s cookbook, KITCHEN 101: Secrets to Cooking Confidence, includes a chapter on Crock Pot Convenience. You will LOVE easy crock pot pork recipes and we think immediately of Holly’s fabulous Cuban Pork and Black Beans recipe.
Crock Pot Cuban Pork and Black Beans
2 pork tenderloins1-pound
1 can black bean soup15-ounce
1 can black beansrinsed and drained, 15-ounce
1 can tomatoes and green chilies10-ounce
1tablespoon chopped jalapeños
2tablespoons ground cumin
2tablespoons lime juice
Season tenderloins heavily with garlic powder. In 3 ½-6-quart slow cooker, insert plastic liner if desired, and mix together remaining ingredients.
Add tenderloins and turn to coat with sauce. Cook on LOW 6-8 hours or until tender.
Terrific Tip: By timing the herbs you will boost flavor — add dried herbs to the slow cooker in beginning of cooking, and fresh herbs just before serving.
Serving Option: Serve over yellow rice.
KITCHEN 101 Highlights Easy Crock Pot And Diabetic Recipes
This easy slow cooker pork loin recipe for Cuban Pork and Black Beans makes one of the most flavorful diabetic pork recipes. There’s no magical diabetes diet and you’ll find we have many of your favorite recipes diabetic friendly.
There are so many diabetic dinner recipes in this cookbook like Holly’s fabulous diabetic pork recipes. In KITCHEN 101 I have a “D” by all diabetic-friendly recipes throughout the book. Cuban Pork and Black Beans recipe meets with the ADA guidelines and is absolutely fantastic
From Crock Pot Pork Recipes to Divine Desserts
With Bananas Foster in the crock pot, serve dinner, and you have a hot, home-cooked fantastic dessert ready at the end of the meal! Crock pot or slow cooker recipes are such a time saver for the busy person. Nothing beats an easy crock pot dinner and a one-dish meal. There is a crock pot symbol indicating crock pot recipes inKITCHEN 101so look for is throughout the cookbook! With a home office you can smell the wonderful aroma cooking all day.
Can you eat delicious food that is also good for you? Of course! Diabetic friendly meals definitely do not have to be boring and tasteless. This Diabetic Meal Plan & Recipes Downloadable is your easy go-to guide to meal planning diabetic meals the whole family will love. This comprehensive guide includes 13 weekly recipes, from dinners, lunch, snacks and dessert.
The prevalence of obesity began to rise rapidly in the 1980s and since then has more than doubled (1). Sugar (2), sugar-sweetened beverages, and the fructose that they provide have been consistently linked to the risk for obesity (3). Ludwig, Peterson, and Gortmaker (4) provided one of the earliest suggestions that intake of sugar-sweetened beverages might predict weight gain, and this has been supported by an increasing number of studies (5). Because foods can activate the “pleasure” center circuitry, the same circuitry that is activated by drugs of abuse and alcohol (6), the suggestion that sugar might be “addictive” has surfaced from time to time (7,8).
The study by Jastreboff et al. in this issue of Diabetes (9), and an earlier pilot study (10), using functional MRI after oral ingestion of either glucose or fructose in 14 lean and 24 adolescents with obesity extends our knowledge of how these hexoses act on the brain. In the lean adolescents, both glucose and fructose increased perfusion of brain areas involved in “executive function and control” (prefrontal cortex) (Fig. 1) but did not activate the “homeostatic” appetite control areas (hypothalamus). A very different picture was seen in the adolescents with obesity where ingestion of either fructose or glucose reduced perfusion of the executive region of the brain (prefrontal cortex) and increased activity in the “reward” or “pleasure” centers. This suggests that obese adolescents may lack the ability to downregulate the hedonic and homeostatic regions of the brain after oral ingestion of fructose or glucose. In addition, the ingestion of fructose produced a greater increase in perfusion of the pleasure or reward centers in the adolescents with obesity—something not seen in the lean adolescents. The authors speculate that the reduced response of the executive centers to fructose/glucose may reduce their ability to control intake of sugar-sweetened beverages.
Signaling in the brain of adolescents in response to glucose or fructose: schematic representation of changes in the periphery and brain after the ingestion of glucose or fructose. Subjective responses using variable analog scales (VAS) are shown in the lower-left corner for hunger, fullness, and satiety where differences were detected. Both glucose and fructose are absorbed, but fructose is largely cleared in the liver, where it stimulates de novo lipogenesis. Glucose is taken up by many tissues and stimulates insulin release from the pancreas more so in the adolescents with obesity than in lean adolescents. Both monosaccharides reduce circulating acyl-ghrelin concentrations. Effects of glucose and fructose on cerebral blood flow relative to baseline are shown by arrows in major regions of the brain: the prefrontal cortex, which has major executive functions; the hypothalamus, which modulates appetite; and the limbic system and striatum-thalamus, which encompass the reward feature of food. Solid lines represent neural connections and dashed lines circulating connections. ‡Adjusted for acyl-ghrelin and insulin. ACC, anterior cingulate cortex; F, fructose; Fru, fructose; G, glucose; GLP-1, glucagon like peptide 1; L, lean adolescents; N. accumbens, nucleus accumbens; Ob, adolescents with obesity; OXM, oxyntomodulin; PP, pancreatic polypeptide; PYY, polypeptide YY; TG, triglyceride.
After absorption, fructose is largely cleared by the liver, leaving only small circulating concentrations. The intriguing question is how fructose produces these effects in the brain. Jastreboff et al. (9) suggest a possible mechanism through changes in the active form of ghrelin (acyl-ghrelin) with a contribution from the higher insulin in the obese. After ingestion of glucose, acyl-ghrelin is significantly suppressed by glucose and more so by fructose in the adolescents with or without obesity. However, circulating levels are higher in the lean than the obese. Changes in ghrelin might provide a signal for the changes in perfusion in various brain regions. Insulin, which responds to glucose, may also play a role through its central nervous system receptors, since the relative increase of insulin in the adolescents with obesity was much greater than in the lean adolescents. However, changes in insulin with fructose were very small, suggesting that lowering of acyl-ghrelin may be a more important messenger for control of central behavior and activation of the pleasure center.
Understanding how adolescents who are obese differ from those who are not is important in framing preventive strategies. The study by Jastreboff et al. (9) describes functional differences in the central nervous system during response to fructose or glucose solutions. First, the executive center in the prefrontal cortex is inhibited in the obese, confirming earlier work in adolescents (11,12) and adults where Volkow et al. (13) showed a significant negative correlation between BMI and metabolic activity in prefrontal cortex and cingulate gyrus. Using leptin as a surrogate for fatness, Jastreboff et al. (9) found that it was inversely related to blood flow in the prefrontal cortex. Second, the hypothalamus, which plays a key role in the homeostatic regulation of food intake, is activated by glucose/fructose in the adolescents with obesity but not in the lean, a change that might stimulate feeding in those with obesity. The pleasure or reward centers in the limbic system and striatum are also activated by fructose/glucose in adolescents with obesity. Much evidence supports the hypothesis that the arcuate hypothalamus plays a direct role in ghrelin-regulated homeostatic feeding and that the ventral tegmental area directly mediates ghrelin-induced hedonic eating (14).
This is a cross-sectional study and leaves at least one key question unanswered: Which came first, the obesity or the changes in brain response? The idea that sugar might be addictive or habituating surfaced over 40 years ago (7,8), in part related to the finding that endogenous opioids (endorphin and enkephalin) stimulate feeding, as do endogenous cannabinoids, which were identified after noting that “marihuana” stimulated feeding.
In addition to the association of sugar (glucose/fructose) intake with the risk for developing obesity, diabetes, and heart disease, fructose seems to have other possibly detrimental metabolic effects (15,16). Fructose stimulates de novo lipogenesis and liver fat (17), increases visceral adipose tissue (16), and increases triglyceride levels (15). Drinking sugar-sweetened beverages for 6 months can replicate the findings of the metabolic syndrome (18). Both glucose and fructose provide energy, but fructose in addition provides a more intense sweetness than glucose and, as shown in the study by Jastreboff et al. (9), stimulates the striatal complex, which may provide a hedonic override of the homeostatic control of feeding (19).
Evidence supporting features of addiction to sucrose come mainly from studies in experimental animals (7). Withdrawal from a “sugar-rich” diet is associated with behavior suggestive of “withdrawal” symptoms. Clinical support for this idea comes from a study by Drewnowski et al. (20), who used naloxone to block opioid receptors in women who were binge eaters and those who were not. In the binge eaters, naloxone reduced the preference for sweet taste and the actual amounts consumed. The findings of Jastreboff et al. (9) that glucose and fructose stimulate the striatal system more in the adolescents with obesity than in lean individuals indicate that these molecules have addictive or habituating potential. In many cases sucrose is consumed in sugar-sweetened beverages that also contain caffeine, a drug that stimulates the central nervous system. It would be of great interest to find out whether caffeine added to the glucose or fructose produced more profound effects on the striatal system of adolescents with obesity.
Duality of Interest. No potential conflicts of interest relevant to this article were reported.
This post may contain affiliate links. Please read our disclosure.
This Cuban braised beef is slow cooked with delicious tomatoes, peppers, and onions for a dish that’s packed with flavor and only takes minutes to prep!
Slow cookers are one of the best ways to cook easy, hearty meals. And this Cuban braised beef may be one of the most flavorful I’ve tried!
In fact, the hardest part is smelling it all day as it cooks. The aroma of beef, veggies, and spices is so alluring, but it’s all worth it once you get to sit down to this delicious plate!
This dish is called Ropa Vieja in Cuba, meaning “old clothes,” because the shredded beef and vegetables look like a heap of colorful rags. Sounds tasty, right?
But trust me: after one bite, you will be ready to dive into this messy pile again and again. There’s the reason it’s the national dish of Cuba!
How to make Cuban braised beef
Slow cookers are amazing at infusing flavor into dishes with very little effort on your part. The only work you have to do is chop, stir, and shred!
Step 1: Combine the tomatoes, oregano, cumin, salt, and pepper in the slow cooker. Mix everything together.
Step 2: Add the bell peppers and onion, then stir again.
Step 3: Nestle the pieces of beef in the vegetables.
Step 4: Cook, covered, until the meat is tender, about 7-8 hours on low or 4-5 hours on high.
Step 5: Without taking the beef out of the pot, shred using two forks.
Step 6: Stir to mix the shredded beef with the liquid and vegetables.
Step 7: Garnish with sliced avocado and chopped cilantro to serve.
How easy is that? Your messy pile of tasty veggies and shredded beef is ready to enjoy!
How to serve braised beef
Traditionally, this dish is served with white rice, black beans, and sometimes maduros.
I like to serve it over brown rice, which has better nutritional value than white rice and is great for soaking up all the extra sauce!
Also, don’t skip the avocado. It really adds a nice pop of flavor and texture to the dish. Plus, it’s a great source of healthy fat!
If you think this Cuban beef is tasty right out of the slow cooker, wait until you try the leftovers! The flavors will deepen in the refrigerator, making it even more hearty and delicious.
Leftovers can be stored in an airtight container in the refrigerator for 3-4 days. If possible, don’t add the avocado to each serving until you’re ready to eat.
Once sliced, avocado will oxidize and turn black. It’s much more appetizing if it’s sliced right before eating.
Other delicious slow cooker recipes
Looking for more easy and flavorful dishes you can throw together in the slow cooker? Here are a few of my favorites that I know you’ll love:
When you’ve tried this dish, please don’t forget to let me know how you liked it and rate the recipe in the comments below!
Cuban Braised Beef
This Cuban braised beef is slow cooked with delicious tomatoes, peppers, and onions for a dish that’s packed with flavor and only takes minutes to prep!
Combine the tomatoes, oregano, cumin, salt, and pepper in the slow cooker. Mix everything together.
Add the bell peppers and onion, then stir again.
Nestle the pieces of beef in the vegetables.
Cook, covered, until the meat is tender, about 7-8 hours on low or 4-5 hours on high.
Without taking the beef out of the pot, shred using two forks.
Stir to mix the shredded beef with the liquid and vegetables.
Garnish with sliced avocado and chopped cilantro to serve.
This recipe is for 6 servings of Cuban slow cooked beef and vegetables. I recommend serving with brown rice to soak up the extra sauce. Leftovers can be stored covered in the refrigerator for 3-4 days.
Nutrition Info Per Serving
Cuban Braised Beef
Amount Per Serving
Calories 302 Calories from Fat 53
% Daily Value*
Saturated Fat 2.6g16%
Polyunsaturated Fat 0.5g
Monounsaturated Fat 3.7g
Net carbs 8.1g
* Percent Daily Values are based on a 2000 calorie diet.