Spinach Dumplings – Diabetic Foodie

By electricdiet / January 21, 2021


These spinach dumplings stuffed with ricotta cheese are the perfect meatless comfort food. You can boil or steam them for an absolutely delicious dish!

Spinach Dumplings in a white bowl topped with tomato sauce and parmesan

I’ve been trying to incorporate more meatless dishes into my weekly menu. So when I found myself craving meatballs, I decided to come up with a vegetarian version.

These spinach dumplings were just what I wanted! They’re stuffed with spinach, ricotta, Parmesan, and Italian seasoning for a delicious, hearty meal.

Add a little pasta sauce on top, and you’ll be craving this bowl of comfort all the time!

One thing to note about this recipe is that the dough needs to chill for 24 hours. So it’s a great dish to use as part of your meal prep on a Sunday.

The rest of the process is very straight-forward. And the dumplings are so delicious, it’s well worth the wait!

How to make spinach dumplings

These tasty bites come together in three phases: making the dough, shaping the dumplings, then cooking the dumplings.

Here are the step-by-step details:

Step 1: In a medium saucepan, combine the frozen spinach and 2 tablespoons of water. Cover and cook over low heat, stirring occasionally, until the spinach is completely thawed, about 15 minutes.

Step 2: Drain the spinach in a strainer and allow to cool.

Step 3: Place the spinach on a clean dish towel or cloth napkin, then grab the corners to form a pouch. Twist to squeeze out as much liquid as possible, then set aside.

Step 4: Beat the eggs in a large bowl.

Step 5: Add the bread crumbs, Italian seasoning, ricotta, Parmesan, scallions, parsley, basil, garlic, nutmeg, and black pepper. Mix well. Add the spinach and mix again until the spinach is well incorporated.

Step 6: Cover and refrigerate for 24 hours.

Step 7: Line two baking sheets with parchment paper. Lightly dust with flour.

Step 8: Take a generous teaspoonful of the chilled dough, roll it into a ball, then place on the prepared baking sheet. Repeat with remaining dough, making sure the dumplings don’t touch.

Step 9: Make a dent in the middle of each dumpling with the end of a wooden spoon or your thumb.

Step 10: Select a saucepan that will fit a bamboo steamer. Fill it half-full with water and bring to a boil.

Step 11: Place the dumplings in a steamer basket, making sure they don’t touch.

Step 12: Place the basket on top of the saucepan and steam over high heat for 10 minutes.

Step 13: Transfer the dumplings to a covered dish to stay warm while you steam the remaining dumplings.

I like to serve mine with oven-roasted tomato sauce and a hearty serving of grated Parmesan!

Dumplings in the steamer basket

Boiling the dumplings

I’ve tried cooking these dumplings both by boiling them and by steaming them. Both versions tasted amazing!

I will say that when I boiled the dumplings, some of them fell apart. They still tasted great, but didn’t look very pretty.

Steaming takes a little longer because you can only cook a few at a time, but they hold their shape better.

If you prefer to boil your dumplings, start by bringing a large pot of water to a boil over high heat. Add half of the dumplings, then reduce the heat to medium.

After about 5 minutes, the dumplings should start to float to the surface. Continue to cook them for another 4 minutes, then use a slotted spoon to drain them and transfer to a covered dish.

Repeat with the remaining dumplings.

Storage

If you have any leftover dumplings, allow them to cool fully before storing them covered in the refrigerator. They will stay fresh for up to 5 days.

You can also store the uncooked dumplings after you shape them. Just keep them covered in the refrigerator.

Then, once you’re ready to eat a few, just steam or boil your desired number of dumplings! That way, you can enjoy them hot and fresh whenever you like.

Other meatless comfort food recipes

Are you trying to incorporate more vegetarian dishes into your diet? There are so many delicious and satisfying recipes out there! Here are a few of my favorites I know you’ll enjoy:

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!

Recipe Card

Spinach dumplings with tomato sauce and parmesan

Spinach Dumplings

These spinach dumplings stuffed with ricotta cheese are the perfect meatless comfort food. You can boil or steam them for an absolutely delicious dish!

Prep Time:15 minutes

Cook Time:40 minutes

Chill Time:1 day

Total Time:1 day 55 minutes

Author:Shelby Kinnaird

Servings:6 servings

Instructions

  • In a medium saucepan, combine the frozen spinach and 2 tablespoons of water. Cover and cook over low heat, stirring occasionally, until the spinach is completely thawed, about 15 minutes.

  • Drain the spinach in a strainer and allow to cool.

  • Place the spinach on a clean dish towel or cloth napkin, then grab the corners to form a pouch. Twist to squeeze out as much liquid as possible, then set aside.

  • Beat the eggs in a large bowl.

  • Add the bread crumbs, Italian seasoning, ricotta, Parmesan, scallions, parsley, basil, garlic, nutmeg, and black pepper. Mix well. Add the spinach and mix again until the spinach is well-incorporated.

  • Cover and refrigerate for 24 hours.

  • Line two baking sheets with parchment paper. Lightly dust with flour.

  • Take a generous teaspoonful of the chilled dough, roll it into a ball, then place on the prepared baking sheet. Repeat with remaining dough, making sure the dumplings don’t touch.

  • Make a dent in the middle of each dumpling with the end of a wooden spoon or your thumb.

  • Select a saucepan that will fit a bamboo steamer. Fill it half-full with water and bring to a boil.

  • Place the dumplings in a steamer basket, making sure they don’t touch.

  • Place the basket on top of the saucepan and steam over high heat for 10 minutes.

  • Transfer the dumplings to a covered dish to stay warm while you steam the remaining dumplings.

Recipe Notes

This recipe is for 6 servings. If you make 48 dumplings total, each serving will be 8 dumplings.
You can choose to steam or boil your dumplings. Steaming takes longer, but they will maintain their shape better.
Extra dumplings can be stored covered in the refrigerator for up to 5 days.
You can also store the uncooked dumplings after you shape them. Keep them covered in the refrigerator until you’re ready to steam or boil them.

Nutrition Info Per Serving

Nutrition Facts

Spinach Dumplings

Amount Per Serving (8 dumplings)

Calories 294
Calories from Fat 108

% Daily Value*

Fat 12g18%

Saturated Fat 6g38%

Trans Fat 0g

Polyunsaturated Fat 0g

Monounsaturated Fat 0g

Cholesterol 101mg34%

Sodium 224mg10%

Potassium 331mg9%

Carbohydrates 29g10%

Fiber 5g21%

Sugar 3g3%

Protein 14g28%

Net carbs 24g

* Percent Daily Values are based on a 2000 calorie diet.

Course: Main Course

Cuisine: Italian

Diet: Diabetic

Keyword: easy dinner recipes, spinach dumplings



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Rainbow Bagels –

By electricdiet / January 19, 2021





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Low-Carb Crab Cakes (Keto) | Diabetes Strong

By electricdiet / January 17, 2021


Ditch the bread crumbs and try these low-carb crab cakes instead! You still get the perfect golden exterior and wonderful crab flavor without all the unwanted carbs or gluten.

Four Low-Carb Crab Cakes on a white plate garnished with chopped parsley

If you ask me, the very best crab cakes are the ones you get in little beach towns on the east coast. Maybe it’s something about the salty breeze, but the ones I’ve ordered at inland restaurants never quite compare.

That being said, whenever the craving strikes, these low-carb crab cakes really hit the spot! The juicy lump crab and crispy golden exterior are so irresistible.

Plus, by eliminating the breadcrumbs and flour that restaurants often use as the binder, we turn crab cakes into a totally keto-friendly dish!

So weather you’re dreaming of a beach vacation or simply find yourself craving some delicious seafood, there’s never a bad time to whip up some tasty crab cakes.

How to make low-carb crab cakes

This easy recipe comes together in just a few simple steps. Start to finish, it only takes about half an hour to make!

Ingredients for crab cakes in separate ramekins, as seen from above

Step 1: In a large mixing bowl, add all of the ingredients for the crab cakes.

Ingredients for crab cakes, unmixed in a glass bowl

Step 2: Mix the ingredients until well-combined.

Crab cake mixture in a glass bowl with a wooden spoon

Step 3: Form the mixture into 4 small patties and chill in the refrigerator for 15 minutes.

Step 4: In a large frying pan over medium-high heat, add the olive oil.

Step 5: Once the oil is hot, add the patties and fry for about 5 minutes per side until they are cooked through and golden brown on each side.

I like to sprinkle mine with fresh parsley and serve with a side of tartar sauce!

How do you make crab cakes without breadcrumbs?

Traditional crab cakes use wheat flours and breadcrumbs to bind the patties together. Unfortunately, both of these options can quickly increase the carb count and add unwanted gluten.

So what makes a good binder for crab cakes in place of those high-carb ingredients?

It’s easy: almond flour!

This simple low carb swap along with the egg and mayonnaise helps the cakes stick together. Plus, it gives them a little extra crunch once they’re fried!

4 crab cakes on a plate garnished with parsley, as seen from above

Storage

These crab cakes can be stored in the refrigerator in an airtight container. They will stay fresh for up to 3 days.

I recommend reheating them in a pan with a little oil to help re-crisp the outside. You can also enjoy them cold!

Other low carb seafood recipes

Seafood and shellfish are great options when you’re sticking to a low-carb diet. There are just so many delicious dishes you can make!

Here are a few of my favorite Keto-friendly seafood recipes I know you’ll love:

I also put together this roundup of healthy low-carb seafood recipes for even more options!

When you’ve tried this crab cake recipe, please don’t forget to let me know how you liked it and rate the recipe in the comments below!

Recipe Card

Low-Carb Crab Cakes

Ditch the bread crumbs and try these low-carb crab cakes instead! You still get the perfect golden exterior and wonderful crab flavor without all the unwanted carbs or gluten.

Prep Time:5 minutes

Cook Time:10 minutes

Chill Time:15 minutes

Total Time:30 minutes

Servings:2

Four Low-Carb Crab Cakes on a white plate garnished with chopped parsley

Instructions

  • In a large mixing bowl, add all of the ingredients for the crab cakes.

  • Mix the ingredients until well-combined.

  • Form the mixture into 4 small patties and chill in the refrigerator for 15 minutes.

  • In a large frying pan over medium-high heat, add the olive oil.

  • Once the oil is hot, add the patties and fry for about 5 minutes per side until they are cooked through and golden brown on each side.

Recipe Notes

This recipe is for 2 servings. Each serving includes 2 crab cakes.
I recommend serving with chopped parsley and tartar sauce.
Leftover crab cakes can be stored in an airtight container in the refrigerator for up to 3 days.

Nutrition Info Per Serving

Nutrition Facts

Low-Carb Crab Cakes

Amount Per Serving (2 crab cakes)

Calories 388
Calories from Fat 244

% Daily Value*

Fat 27.1g42%

Saturated Fat 4.1g21%

Trans Fat 0g

Polyunsaturated Fat 7.7g

Monounsaturated Fat 10.6g

Cholesterol 264mg88%

Sodium 1806.7mg75%

Potassium 193.3mg6%

Carbohydrates 7.4g2%

Fiber 2.7g11%

Sugar 3.2g4%

Protein 31.1g62%

Net carbs 4.7g

* Percent Daily Values are based on a 2000 calorie diet.

Course: Main Course

Cuisine: American

Keyword: crab, crab cake, gluten-free, low carb



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Easy Crock Pot Pork Recipes- Delicious Diabetic Cuban Pork and Black Beans

By electricdiet / January 15, 2021


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 picmonkey

Crock Pot Cuban Pork and Black Beans

    Servings8 servings

    Ingredients

    • 2


      pork tenderloins1-pound



    • garlic powder

    • 2


      onionschopped

    • 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

    Instructions
    1. Season tenderloins heavily with garlic powder. In 3 ½-6-quart slow cooker, insert plastic liner if desired, and mix together remaining ingredients.

    2. Add tenderloins and turn to coat with sauce. Cook on LOW 6-8 hours or until tender.

    Recipe Notes

    Calories 245 Calories from Fat 23% Fat 6g Saturated Fat 2g Cholesterol 76mg Sodium 527mg Carbohydrates 17g Dietary Fiber 5g Total Sugars 5g Protein 29g, Dietary Exchanges: 1 starch, 1 vegetable, 4 lean meat

    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 in KITCHEN 101 so look for is throughout the cookbook! With a home office you can smell the wonderful aroma cooking all day.

    Slow Cooker Liners are a Must!

    Reynolds Slow Cooker Liners 2 Pack (8 Liners Total)Reynolds Slow Cooker Liners 2 Pack (8 Liners Total)Reynolds Slow Cooker Liners 2 Pack (8 Liners Total)Heavy-duty Crockpot Liners BPA-free Made in the USA, 8 Liners 13Heavy-duty Crockpot Liners BPA-free Made in the USA, 8 Liners 13Heavy-duty Crockpot Liners BPA-free Made in the USA, 8 Liners 13PanSaver 12 Pack Disposable Slow Cooker LinersPanSaver 12 Pack Disposable Slow Cooker LinersPanSaver 12 Pack Disposable Slow Cooker Liners

    Simplify Weekly Meal Planning with Holly’s Diabetic Meal Plan Downloadable

    diabetic meal plan

    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.

    Get All of Holly’s Healthy Easy Cookbooks

    The post Easy Crock Pot Pork Recipes- Delicious Diabetic Cuban Pork and Black Beans appeared first on The Healthy Cooking Blog.



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    SGLT2 Inhibition for CKD and Cardiovascular Disease in Type 2 Diabetes: Report of a Scientific Workshop Sponsored by the National Kidney Foundation

    By electricdiet / January 13, 2021


    Article Information

    Acknowledgments. The authors thank the conference participants, who aside from the authors of this article included: Amanda Adler, MD, PhD, Oxford, U.K.; Maryam Afkarian, MD, PhD, Sacramento, CA; Radica Alicic, MD, Spokane, WA; Meaghan Allain, Falls Church, VA; Pamela Anderson, MBA, Titusville, NJ; George Bakris, MD, Chicago, IL; Petter Bjornstad, MD, Aurora, CO; Jaime Blais, PhD, Titusville, NJ; Glenn Chertow, MD, MPH, Palo Alto, CA; Alfred Cheung, MD, Salt Lake City, UT; Mihye (Mia) Cmiel, PharmD, Philadelphia, PA; Stephanie Cogan, New York, NY; Mark Cooper, MBBS, PhD, Melbourne, Australia; Kerry Cooper, MD, Gaithersburg, MD; Ian de Boer, MD, MS, Seattle, WA; Luca De Nicola, MD, PhD, Naples, Italy; Ralph Defronzo, MD, San Antonio, TX; Tony Deluzio, Bridgewater, NJ; Barbara Gillespie, MD, MMS, Chapel Hill, NC; Anthony Gucciardo, New York, NY; Michelle Hangey, BBA, MBA, Philadelphia, PA; Raymond Harris, MD, Nashville, TN; Sibylle Hauske, MD, MBA, Ridgefield, CT; Richard Haynes, DM, MRCP, Oxford, U.K.; Will Herrington, MA, MBBS, MD, Oxford, U.K.; Donna Hodge, Titusville, NJ; Diana Jalal, MD, Iowa City, IA; Meg Jardine, MBBS, PhD, Sydney, Australia; Nichole Jefferson, Dallas, TX; Steven Kahn, MBChB, Seattle, WA; Mikhail Kosiborod, MD, Kansas City, MO; Liz Leff, New York, NY; Kerry Leigh, RN, Washington DC; Helen Looker, MBBS, MRCP, Phoenix, AZ; Julie Lovshin, MD, PhD, Ontario, Canada; Sally Marshall, MD, Tyne, U.K.; Julie Maurey, PharmD, Philadelphia, PA; Peter McCullough, MD, MPH, Dallas, TX; Jim McDermott, PhD, Gaithersburg, MD; Ciaran McMullan, MB BCh, MMSc, Philadelphia, PA; Elizabeth Montgomery, New York, NY; Marcel H. Muskiet, MD, Amsterdam, the Netherlands; Robert Nelson, MD, PhD, Phoenix, AZ; Joshua Neumiller, PharmD, Pullman, WA; Susanne Nicholas, MD, MPH, PhD, Los Angeles, CA; Gregorio Obrador, MD, MPH, Mexico City, Mexico; Milton Packer, MD, Dallas, TX; Sachin Paranjape, PhD, Bridgewater, NJ; Meda Pavkov, MD, PhD, Atlanta, GA; Pablo Pergola, MD, PhD, San Antonio, TX; Michaela Petrini, PA-C, MHS, Ridgefield, CT; Glenda Roberts, Seattle, WA; Motoaki Sano, MD, PhD, Tokyo, Japan; Jay Shubrook, DO, Vallejo, CA; Anna Solini, MD, PhD, Pisa, Italy; Christopher Sorli, MD, PhD, Bridgewater, NJ; Paul Strumph, MD, Durham, NC; Merlin Thomas, MBChB, PhD, Melbourne, Australia; Aliza Thompson, MD, Silver Spring, MD; Marcello Tonelli, MD, Edmonton, Alberta, Canada; Robert Toto, MD, Dallas, TX; Daniel van Raalte, MD, PhD, Amsterdam, the Netherlands; Joseph Vassalotti, MD, New York, NY; Mark West, PharmD, Pittsburgh, PA; Ernest W. Wright, PhD, DSci, FRS, Los Angeles, CA; Jason Wright, PharmD, Gaithersburg, MD; and Helen Yeh, PhD, Gaithersburg, MD. The authors thank Emily J. Cox, PhD (Providence Health Care, Providence Medical Research Center, Spokane, WA) who assisted in the development of Fig 3.

    Support. The following companies provided a grant to the NKF to support the planning and conduct of the workshop: AstraZeneca, Boehringer Ingelheim, Janssen, Sanofi, Merck, and Metavant.

    The workshop sponsors had no role in the development of the workshop agenda or objectives. The sponsors were restricted from viewing any part of the workshop report manuscript until it was accepted for publication and therefore had no role in the content developed for this report.

    Financial Disclosure. K.R.T. is supported by National Institutes of Health (NIH) grants and a Centers for Disease Control and Prevention contract and has served as a consultant for Eli Lilly & Co, Boehringer Ingelheim, AstraZeneca, Gilead, Goldfinch Bio, Novo Nordisk, Bayer, and Janssen. M.A.C. has received research support (nonsalary) from Amgen, AstraZeneca, Bristol Myers Squibb, Chiesi, CSL Behring, GlaxoSmithKline, and Novartis; research support (salary) from Novo Nordisk; and consulting fees from AstraZeneca, Boehringer Ingelheim, Boston Scientific, Edwards Lifesciences, and Merck. L.P. has received personal fees from speaking and/or consulting from Novo Nordisk, Sanofi, AstraZeneca, Boehringer Ingelheim, Janssen, Merck, and UpToDate. V.V. reports grants from the NIH and has served as a consultant and received honoraria from Bayer, Boehringer Ingelheim, Eli Lilly & Co, Janssen Pharmaceutical, Merck, and Retrophin and grant support for investigator-initiated research from AstraZeneca, Bayer, Boehringer Ingelheim, Fresenius, and Janssen Pharmaceutical. P.R. reports having given lectures for AstraZeneca, Bayer, Novo Nordisk, and Boehringer Ingelheim and has served as a consultant for AbbVie, AstraZeneca, Bayer, Eli Lilly & Co, Boehringer Ingelheim, Astellas, Gilead, Mundipharma, Vifor, and Novo Nordisk, all fees given to Steno Diabetes Center Copenhagen. F.C.B. reports grants from the NIH and the Juvenile Diabetes Research Foundation; the University of Michigan has contracted with Gilead for his consulting services. P.F. reports receiving personal fees for advisory boards or scientific presentations from AstraZeneca, Mundipharma, Boehringer Ingelheim, Eli Lilly & Co, and Novartis. K.J.F. is a consultant for Responsum Health, Bayer, Gilead, Chiesi, Talaris, Retrophin, Otsuka, and Veloxis. H.J.L.H. has served as a consultant for Abbvie, AstraZeneca, Boehringer Ingelheim, Fresenius, Gilead, Janssen, Merck, Mundipharma, Mitsubishi-Tanabe, and Retrophin and received grant support from Abbvie, AstraZeneca, Boehringer Ingelheim, and Janssen. A.K.M. has contracts with Aurinia, Boehringer Ingelheim, Calliditas, Duke Clinical Research Institute, and Pfizer; has been a member of the scientific advisory board for AstraZeneca; and has consultancy agreements with Proteomics Int. S.E.R. reports grants from the NIH, Bayer, and Ironwood Pharmaceuticals and has participated in advisory boards for Reata and Bayer Healthcare. M.E.M. reports grants from the National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Novartis, and Novo Nordisk and consulting fees from Merck, Pfizer, and Janssen. D.K.M. has received honoraria for clinical trial leadership from AstraZeneca, Sanofi Aventis, Janssen, Boehringer Ingelheim, Merck & Co, Pfizer, Novo Nordisk, Lexicon, Eisai Inc, GlaxoSmithKline, Lilly USA, and Esperion and honoraria for consultancy from AstraZeneca, Sanofi Aventis, Lilly USA, Boehringer Ingelheim, Merck & Co, Novo Nordisk, Metavant, Applied Therapeutics, and Afimmune. C.W. has received honoraria from AstraZeneca, Sanofi, Boehringer Ingelheim, Merck, Eli Lilly & Co, and Mundipharma. T.M. is employed by the NKF. V.P. has received fees for advisory boards, steering committee roles, or scientific presentations from Abbvie, Astellas, AstraZeneca, Bayer, Baxter, BMS, Boehringer Ingelheim, Chinook, Dimerix, Durect, Eli Lilly & Co, Gilead, GSK, Janssen, Merck, Mitsubishi Tanabe, Mundipharma, Novartis, Novo Nordisk, Pfizer, Pharmalink, Relypsa, Retrophin, Sanofi, Servier, Vifor, and Tricida.



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    Peach Chia Jam (No Added Sugar)

    By electricdiet / January 11, 2021


    Have you ever tried making jam in your Instant Pot? This tasty peach chia jam is thickened with nutrient-rich chia seeds and has no added sugar!

    Peach Chia Jam in a glass jar on a wooden cutting board next to dry chia seeds and peach slices

    I recently came across two ideas that I found very intriguing. The first was to make jam in your Instant Pot, and the second was to use chia seeds to thicken your jam.

    So I decided to combine them into this tasty peach chia jam! It’s a delicious way to use up extra peaches, and you can make the whole recipe right in your electric pressure cooker.

    I love how you get a nutrient boost from the chia seeds! They’re packed with omega-3 fatty acids, antioxidants, fiber, calcium, and iron, and they may improve insulin sensitivity and reduce inflammation.

    If some guilt-free, no-sugar-added peach jam sounds like a treat, just wait until you try a bite!

    How to make peach chia jam

    To make this tasty, sugar-free peach jam, all you need is an electric pressure cooker and an immersion blender.

    Step 1: In a 6-quart electric pressure cooker, stir together the peaches, lemon juice, vanilla extract, and almond extract.

    Step 2: Close and lock the lid of the pressure cooker. Ensure the valve is set to “sealing,” then select HIGH manual pressure and set the timer for 2 minutes.

    Step 3: Once the cooking time is up, allow the pressure to release naturally for 15 minutes, then quick release the remaining pressure. When the pressure gauge drops, remove the lid and set it aside.

    Step 4: Use an immersion blender to purée the peach mixture right in the pot.

    Step 5: Stir in the chia seeds, then hit Sauté. Select the “low” setting if your pressure cooker gives you the option.

    Step 6: Stir constantly for about 5 minutes or until the jam has reached the consistency you like.

    Step 7: Hit Cancel to turn off the heat, then allow the jam to cool to room temperature before transferring to a jar.

    Once you try this peach jam made with chia seeds, you may never want the store-bought stuff again!

    Ways to enjoy your jam

    This tasty peach jam is great as part of a diabetic-friendly breakfast, dessert, or snack. There are so many ways to enjoy it!

    Have some leftover whole wheat flax rolls? Cut one in half, slather it with jam, and enjoy with a cup of coffee for breakfast.

    Or, for a high-protein breakfast, whip up a batch of the cottage cheese pancakes from DiabetesStrong.com. Then add a tablespoon or two of peach jam on top!

    You could also add a dollop of jam to plain Greek yogurt or vanilla ice cream. For a similar creamy treat, swirl it into your favorite smoothie.

    There’s no wrong way to enjoy this healthy peach jam!

    Storage

    Once the jam has cooled after cooking, transfer it to a jar with a screw top lid. You can store in the refrigerator for up to 2 weeks.

    For longer storage, the jam will also keep in the freezer for up to 6 months. Make sure to thaw the jam in the refrigerator before using.

    Spoonful of Peach Chia Jam above glass of jam

    Other healthy and fruity recipes

    Looking for more sweet and fruity options you can enjoy as a guilt-free breakfast, snack, or dessert? Here are a few of my favorite recipes I know you’ll love:

    When you’ve tried this jam, please don’t forget to let me know how you liked it and rate the recipe in the comments below!

    Recipe Card

    Peach Chia Jam in a glass jar on a wooden cutting board next to dry chia seeds and peach slices

    Peach Chia Jam (No Added Sugar)

    Have you ever tried making jam in your Instant Pot? This tasty peach chia jam is thickened with nutrient-rich chia seeds and has no added sugar!

    Prep Time:10 minutes

    Cook Time:10 minutes

    Pressure Up/Down Time:25 minutes

    Total Time:45 minutes

    Author:Shelby Kinnaird

    Servings:24

    Instructions

    • In a 6-quart electric pressure cooker, stir together the peaches, lemon juice, vanilla extract, and almond extract.

    • Close and lock the lid of the pressure cooker. Ensure the valve is set to “sealing,” then select HIGH manual pressure and set the timer for 2 minutes.

    • Once the cooking time is up, allow the pressure to release naturally for 15 minutes, then quick release the remaining pressure. When the pressure gauge drops, remove the lid and set it aside.

    • Use an immersion blender to purée the peach mixture right in the pot.

    • Stir in the chia seeds, then hit Sauté. Select the “low” setting if your pressure cooker gives you the option.

    • Stir constantly for about 5 minutes or until the jam has reached the consistency you like.

    • Hit Cancel to turn off the heat, then allow the jam to cool to room temperature before transferring to a jar.

    Recipe Notes

    This recipe is for 24 servings of jam. Each serving is 2 tablespoons.
    If you don’t have any almond extract, just use vanilla extract (2 teaspoons total).
    Store the jam in an airtight container in the refrigerator for up to 2 weeks or in the freezer for up to 6 months. Thaw in the refrigerator before using.

    Nutrition Info Per Serving

    Nutrition Facts

    Peach Chia Jam (No Added Sugar)

    Amount Per Serving (2 tablespoons)

    Calories 20
    Calories from Fat 7

    % Daily Value*

    Fat 0.8g1%

    Saturated Fat 0.1g1%

    Trans Fat 0g

    Polyunsaturated Fat 0.6g

    Monounsaturated Fat 0.1g

    Cholesterol 0mg0%

    Sodium 0.5mg0%

    Potassium 9.8mg0%

    Carbohydrates 3.2g1%

    Fiber 1.1g5%

    Sugar 1.9g2%

    Protein 0.7g1%

    Vitamin A 150IU3%

    Vitamin C 4.1mg5%

    Calcium 150mg15%

    Iron 0.2mg1%

    Net carbs 2.1g

    * Percent Daily Values are based on a 2000 calorie diet.

    Course: Breakfast, Condiments

    Cuisine: American

    Diet: Diabetic

    Keyword: peach chia jam, peach jam, sugar-free peach jam



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    Turkey Burger Parmesan Sliders – %

    By electricdiet / January 9, 2021





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    Keto Shrimp Stir Fry | Diabetes Strong

    By electricdiet / January 7, 2021


    When you need an easy weeknight meal, this tasty keto shrimp stir fry takes less than half an hour to make. Plus, it’s packed with healthy protein and nutrients!

    Stir fry served in two white bowls with forks, as seen from above

    Looking for an easy weeknight meal that’s low in carbs, packed with lean protein and veggies, and takes less than half an hour to make?

    Then you have to try this keto shrimp stir fry! Savory shrimp with crisp snow peas, bell peppers, and thinly-sliced carrots come together for a bowl that is simply irresistible.

    Not to mention, the entire dish is made in one pan! So cooking is simple and clean-up is a breeze. Just what everyone needs on a busy weeknight, right?

    So when you want something healthy that’s bursting with flavor and can be ready in a snap, I highly recommend giving this low carb dish a try.

    How to make keto shrimp stir fry

    This tasty one-pan meal comes together in just 8 simple steps.

    Stir fry ingredients in separate ramekins, as seen from above

    Step 1: In a large pan over medium heat, heat the butter until melted.

    Step 2: Add the shrimp, salt, and pepper, then stir. Cook for 5 minutes, stirring occasionally, until the shrimp are cooked through and light pink.

    shrimp cooking in the skillet

    Step 3: Remove the shrimp from the pan.

    Step 4: In the same pan over medium-high heat, add the sesame oil. Once hot, add the vegetables, tamari, and rice vinegar.

    Step 5: Cook for another 7 – 10 minutes until the vegetables are cooked.

    Step 6: Add the garlic and ginger, then mix well. Add salt to taste if desired.

    Step 7: Add the shrimp back to the pan and stir to combine with the other ingredients.

    Stir fry in skillet, as seen from above

    Step 8: Garnish with chopped green onions and sesame seeds before serving.

    That’s it! Your healthy low carb dinner is ready to enjoy.

    Close-up of stir fry in a white bowl with a fork

    Is shrimp good for keto?

    Shrimp, like most seafood, is a great source of lean protein. But is it a good ingredient for someone following a keto way of eating?

    In fact, there is only 1 gram of carbs per cup of cooked shrimp. So I would say YES, this shellfish is a great option for anyone watching their carbs!

    That same serving size also packs in 24 grams of protein. Not to mention, shrimp are rich in nutrients like zinc, magnesium, iron, and more.

    Thanks to its nutritional profile and very low carb content, shrimp makes a great protein for any keto or low carb meal.

    Storage

    Stir fry is always best when it’s hot out of the pan (or wok). But if you find yourself with leftovers, don’t let them go to waste!

    Simply store them in an airtight container in the refrigerator. I recommend enjoying your leftovers within 3 days.

    Close-up of stir fry in a white bowl with a fork

    Other low carb seafood recipes

    Seafood is such a great option for high-protein, low-carb meals. If you’re looking for more ideas, here are a few of my favorite keto seafood recipes I know you’ll enjoy:

    You can also check out this roundup of healthy low-carb seafood recipes for even more options!

    When you’ve tried this stir fry recipe, please don’t forget to let me know how you liked it and rate the recipe in the comments below!

    Recipe Card

    Keto Shrimp Stir Fry

    When you need an easy weeknight meal, this tasty keto shrimp stir fry takes less than half an hour to make. Plus, it’s packed with healthy protein and nutrients!

    Prep Time:10 minutes

    Cook Time:15 minutes

    Total Time:25 minutes

    Servings:4

    Keto shrimp stir fry in a white bowl with a spoon

    Instructions

    • In a large pan over medium heat, heat the butter until melted.

    • Add the shrimp, salt, and pepper, then stir. Cook for 5 minutes, stirring occasionally, until the shrimp are cooked through and light pink.

    • Remove the shrimp from the pan.

    • In the same pan over medium-high heat, add the sesame oil. Once hot, add the vegetables, tamari, and rice vinegar.

    • Cook for another 7 – 10 minutes until the vegetables are cooked.

    • Add the garlic and ginger, then mix well. Add salt to taste if desired.

    • Add the shrimp back to the pan and stir to combine with the other ingredients.

    • Garnish with chopped green onions and sesame seeds before serving.

    Recipe Notes

    This recipe is for 4 servings of stir fry.
    To lower the carbs, reduce or omit the carrots.
    Leftovers can be stored in an airtight container in the refrigerator for up to 3 days.

    Nutrition Info Per Serving

    Nutrition Facts

    Keto Shrimp Stir Fry

    Amount Per Serving

    Calories 231
    Calories from Fat 95

    % Daily Value*

    Fat 10.6g16%

    Saturated Fat 3.7g19%

    Trans Fat 0g

    Polyunsaturated Fat 1.8g

    Monounsaturated Fat 2.1g

    Cholesterol 172.5mg58%

    Sodium 1006.9mg42%

    Potassium 469.2mg13%

    Carbohydrates 14g5%

    Fiber 7.3g29%

    Sugar 6g7%

    Protein 18.7g37%

    Net carbs 6.7g

    * Percent Daily Values are based on a 2000 calorie diet.

    Course: Main Course

    Cuisine: American

    Keyword: gluten-free, Grilled shrimp, low carb, shrimp stir fry, stir-fry



    Sell Unused Diabetic Strips Today!

    Linking Kidney and Cardiovascular Complications in Diabetes—Impact on Prognostication and Treatment: The 2019 Edwin Bierman Award Lecture

    By electricdiet / January 5, 2021


    Abstract

    In diabetes, increasing albuminuria and decreasing glomerular filtration rate are hallmarks of chronic kidney disease in diabetes and increase the risk of atherosclerotic cardiovascular events and mortality as well as the risk for end-stage kidney disease. For two decades, standard of care has been controlling risk factors, such as glucose, blood pressure, lipids, and lifestyle factors, and specifically use of agents blocking the renin-angiotensin system. This has improved outcome, but a large unmet need has been obvious. After many failed attempts to advance the therapeutic options, the past few years have provided several new promising treatment options such as sodium–glucose cotransporter 2 inhibitors, endothelin receptor antagonists, glucagon-like peptide 1 agonists, and nonsteroidal mineralocorticoid receptor antagonists. The benefits and side effects of these agents demonstrate the link between kidney and heart; some have beneficial effects on both, whereas for other potentially renoprotective agents, development of heart failure has been a limiting factor. They work on different pathways such as hemodynamic, metabolic, inflammatory, and fibrotic targets. We propose that treatment may be personalized if biomarkers or physiological investigations assessing activity in these pathways are applied. This could potentially pave the way for precision medicine, where treatment is optimized for maximal benefit and minimal adverse outcomes. At least it may help prioritizing agents for an individual subject.

    Introduction

    The global burden of diabetes is currently estimated to affect 463 million individuals, or 1 in 11, according to the International Diabetes Federation, and projections suggest a 48% increase in the prevalence to 700 million people by 2045 (1). Diabetes is associated with a two- to fourfold increased risk for atherosclerotic cardiovascular disease (CVD) compared with the background population, and 30–40% with diabetes are affected by chronic kidney disease characterized by increased albuminuria or decreased glomerular filtration rate (GFR) (or diabetic kidney disease [DKD]). The presence of kidney disease increases the risk of CVD, and the combination is a deadly cocktail. Increasing albuminuria or decreasing GFR increases the risk of CVD and mortality (2) (see Fig. 1) as well as the risk for end-stage kidney disease. Furthermore, albuminuria and GFR levels form the basis on which chronic kidney disease is staged according to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines (3). Early-onset DKD may shorten life expectancy by 14–16 years (4), and excess mortality in diabetes is primarily due to mortality in DKD (5), with a 6-fold increased risk for mortality with albuminuria and 15-fold increased risk with albuminuria and reduced GFR (5).

    Figure 1
    Figure 1

    Declining eGFR and increasing albuminuria are associated with mortality in individuals with diabetes. ACR, albumin-to-creatinine ratio (2).

    The aim of this review is to discuss the link between kidney and heart in diabetes, as it is important to understand for optimal treatment and prevention of late complications. Deckert et al. (6) formulated the Steno hypothesis, suggesting that albuminuria reflects widespread vascular damage and proposing a linkage between DKD and CVD. Here, we will discuss recent investigations of functional links showing connections between kidney and heart damage. We will evaluate biomarkers ranging from albuminuria to omics, which could pave the way to a personalized medicine approach in kidney and heart diseases. Finally, we will describe how these biomarkers can be used when applying new therapies such as sodium–glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1RA), and mineralocorticoid receptor antagonists. These agents have different mechanisms of action, and the biomarkers can help tailoring treatment to the pathophysiology. The cardio-renal link is stressed by the fact that some of these agents may work on the kidney to “save” the heart and others protect the kidney but with a risk for heart failure.

    Investigations of Functional Links—Connections Between the Kidney and Heart

    A chronic cardio-renal syndrome has been described where impaired renal function with retention of uremic solutes, hypertension, fluid retention, and anemia affect the heart. On the other hand, a failing heart with low cardiac output with hypoperfusion and atherosclerosis has detrimental impact on renal function (7). In diabetes, the coexistence of microvascular and macrovascular complications increases mortality, and we aimed to investigate the associations between albuminuria and vascular and ventricular function of the heart.

    Major advances in noninvasive imaging enable the investigation of new aspects of the cardiac microcirculation. Among these methods is quantitative cardiac positron emission tomography (PET), which allows measurement of myocardial blood flow at rest and during pharmacologically induced hyperemic conditions. The ratio between flow in the two situations is termed the myocardial flow reserve and mirrors the function of the large epicardial arteries and the microcirculation of the myocardium. Thus, in individuals without epicardial coronary stenosis, cardiac PET can be used to assess the function of the microcirculation, including the combined function of cells in the vascular smooth muscle and endothelial cells. A higher myocardial flow reserve represents enhanced ability to increase the myocardial blood flow under stress.

    A hybrid scanner can combine cardiac PET with computed tomography (CT), enabling the simultaneous estimation of the coronary artery calcium score. A high coronary artery calcium score can identify asymptomatic individuals who are at higher risk of coronary heart disease and mortality (8) and is a specific marker of atherosclerosis, independent of its etiology.

    In the past, clinical use of cardiac PET/CT was limited by the requirement of an expensive PET/CT scanner and an on-site cyclotron for radioisotope production. The development of less expensive PET/CT scanners has resulted in a wider clinical application of cardiac PET/CT. Moreover, rubidium-82 (82Rb) is a PET myocardial perfusion tracer produced with a strontium-82 (82Sr)/82Rb generator and therefore can be used in centers without immediate access to an on-site cyclotron. PET myocardial perfusion imaging with 82Rb has several other advantages including high image quality and low radiation dose as well as rapid examination time. Therefore, cardiac 82Rb PET/CT has replaced the classical myocardial scintigraphy with single-photon emission CT as routine examination for individuals with suspected cardiac ischemia.

    Taking advantage of cardiac 82Rb PET/CT, we have conducted two cross-sectional studies. We aimed to gain information on the prevalence of reduced myocardial flow reserve and increased coronary artery calcium score in individuals with type 1 diabetes and type 2 diabetes (with or without albuminuria as a measure of renal and microvascular damage) while comparing them with healthy control subjects. Moreover, we wanted to examine the association between the myocardial flow reserve and the coronary artery calcium score.

    The first study included 60 individuals with type 2 diabetes, but free of overt CVD, stratified by presence/history of albuminuria (≥30 mg/24 h) (n = 30) or normoalbuminuria (<30 mg/24 h) (n = 30), and 30 age- and sex-matched healthy control subjects (9). The second study comprised 60 individuals with type 1 diabetes stratified by presence/history of macroalbuminuria (≥300 mg/g; n = 30) or normoalbuminuria (<30 mg/g; n = 30) (10). Different cutoff values to define reduced myocardial flow reserve have been applied depending on the characteristic of the study population, and a cutoff of 2.5 has been suggested in individuals without obstructive coronary artery disease (11). We therefore prespecified a cutoff of 2.5. An elevated coronary artery calcium score was defined as an Agatston score >300.

    Cardiac PET/CT in Control Subjects and in Participants With Type 1 or Type 2 Diabetes Stratified by Urinary Albumin Excretion

    Table 1 summarizes the sex, age, level of albuminuria, and main results from the cardiac PET/CT scans in the participants, grouped into control subjects and individuals with type 1 or type 2 diabetes (stratified by urinary albumin excretion level).

    Table 1

    Myocardial flow rate reduced and coronary artery calcium score elevated in type 1 and type 2 diabetes subjects with albuminuria compared with subjects with normoalbuminuria or control subjects

    The main findings in type 1 diabetes were as follows:

    • 1) Myocardial microvascular function was comparable in the healthy control subjects and the individuals with type 1 diabetes and normoalbuminuria but impaired in the presence of macroalbuminuria (see Fig. 2). This indicates that there is a separate microvascular injury in the heart of individuals with type 1 diabetes and albuminuria compared with normoalbuminuria.

    • 2) Coronary calcification was higher in individuals with type 1 diabetes compared with healthy control subjects.

    • 3) Coronary calcification was comparable in normo- and macroalbuminuric individuals with type 1 diabetes; however, when coronary artery calcium score was dichotomized, the frequency of elevated coronary artery calcium score (>300) was higher in individuals with macro- compared with normoalbuminuria. Therefore, it might be that there is an association between coronary artery calcium score and albuminuria in type 1 diabetes, but that we had limited power to detect it because of a skewed distribution of the coronary artery calcium scores.

    Figure 2
    Figure 2

    Myocardial flow reserve (MFR) associated with albuminuria (urinary albumin-to-creatinine ratio [UACR]) in type 1 diabetes (10).

    The main findings in type 2 diabetes were as follows:

    • 1) Myocardial microvascular function was impaired in individuals with type 2 diabetes and normoalbuminuria compared with healthy control subjects.

    • 2) Myocardial microvascular function was impaired in the presence of albuminuria compared with normoalbuminuria, and 83% of individuals with albuminuria had impaired myocardial flow reserve (<2.5) compared with 40% with normoalbuminuria.

    • 3) Coronary calcification was higher in individuals with type 2 diabetes compared with healthy control subjects and in individuals with type 2 diabetes and albuminuria compared with normoalbuminuria.

    The Relationship Between Cardiac Vascular Function and Atherosclerosis

    For both type 1 and type 2 diabetes, we demonstrated a significant, but modest, negative correlation between myocardial flow reserve and coronary artery calcium score (R2 = 0.20, P < 0.001 [10], and R2 = 0.24, P < 0.001 [9], respectively). Thus, the relationship between functional changes (myocardial flow reserve) and anatomical features of atherosclerosis (coronary artery calcium score) may not be straightforward and these measures might expose different pathophysiological processes and differences in time course. This implies that a coronary artery calcium score of 0 cannot solely be used as a gatekeeper, as we measured myocardial flow reserves ranging from 1.8 to 4.9 in individuals with a coronary artery calcium score of 0 (9).

    The Relationship Between Cardiac Vascular Function and Cardiac Autonomic Dysfunction

    Cardiac autonomic neuropathy is a severe and often overlooked complication in diabetes associated with kidney disease, increased mortality, and silent myocardial ischemia. Cardiac autonomic dysfunction, including loss of cardiac sympathetic integrity, may contribute to impaired myocardial blood flow regulation.

    The cardiac autonomic function can be evaluated with simple bedside tests using heart rate variability indices or response in heart rate to standing, slow breathing, or the Valsalva maneuver (cardiovascular autonomic reflex tests). These indirect tests can reveal altered sympathetic and parasympathetic activity. Cardiac radionuclide imaging using the nonmetabolized norepinephrine analog metaiodobenzylguanidine (MIBG) allows a direct assessment of the integrity of the adrenergic cardiac innervation and may be more reliable for evaluation of cardiac autonomic function and might also diagnose cardiovascular autonomic neuropathy in early clinical stages before it can be detected by the indirect tests.

    In the two cross-sectional studies described above, we evaluated the association between the cardiac autonomic function and the cardiac vascular function (assessed as the myocardial flow reserve). The cardiac autonomic function was evaluated with use of cardiac MIBG imaging, heart rate variability indices, and cardiovascular autonomic reflex tests (12,13).

    In both studies, we demonstrated that impaired function of the cardiac autonomic system correlated with lower myocardial flow reserve. The association was strongest when the cardiac autonomic function was evaluated with cardiac MIBG imaging, as it persisted after comprehensive adjustment (12,13).

    Cardiac Autonomic Function in Control Subjects and in Participants With Type 1 or Type 2 Diabetes Stratified by Urinary Albumin Excretion

    We demonstrated a general impaired function of the cardiac autonomic system in individuals with type 1 or type 2 diabetes and normoalbuminuria as compared with healthy control subjects (12,13). Compared with participants with normoalbuminuria, individuals with albuminuria had similar cardiac autonomic function assessed by the cardiac MIBG imaging and the heart rate variability indices in type 1 and type 2 diabetes. However, cardiac autonomic neuropathy was more frequent in the participants with albuminuria compared with in those with normoalbuminuria when evaluated by the cardiac autonomic reflex tests.

    Ongoing Study: Myocardial Flow Reserve as Risk Marker

    As the myocardial flow reserve estimates the microvascular function of the heart, it may provide unique risk information beyond the extent of coronary atherosclerosis, and identification of early stages of coronary microvascular disease may provide new prospects for risk stratification.

    The predictive value of the myocardial flow reserve has been evaluated for mortality outcomes in individuals with diabetes (mix of type 1 and type 2) referred for cardiac 82Rb PET/CT due to chest pain or dyspnea. More than 60% had previous CVD and the baseline examination was in 2006–2010, before modern multifactorial treatment, including SGLT2 inhibitors and GLP-1RA, was established (14). The study demonstrated that impaired myocardial flow reserve (<1.6) was associated with a higher rate of cardiac death (14). However, the predictive value of myocardial flow reserve for CVD and mortality in asymptomatic individuals with diabetes remains to be investigated. Therefore, we are conducting a prospective study with the primary aim of identifying subpopulations at high risk of developing CVD during follow-up, among asymptomatic individuals with type 2 diabetes, using myocardial flow reserve and coronary artery calcium score.

    Heart Failure and Association With Microvascular Damage

    In recent years, there has been increasing focus on heart failure in diabetes, as this is associated with a poor prognosis. Heart failure is particularly common in subjects with type 2 diabetes and kidney disease (15) but is also a concern in type 1 diabetes (16). To study whether systolic dysfunction could be detected in individuals with type 1 diabetes without known ischemic heart disease, we conducted a study with echocardiography measuring global longitudinal strain (GLS) as a sensitive measure of systolic function in 1,065 individuals with type 1 diabetes (17). Compared with 198 healthy control subjects, there was a significantly impaired systolic function (GLS) in diabetes. However, for subjects with normoalbuminuria there were no difference when compared with healthy control subjects, whereas presence of micro- or macroalbuminuria was associated with increasingly impaired GLS, again highlighting a link between the kidney (albuminuria) and heart. In evaluations after 7.5 years of follow-up, measures of systolic and diastolic function predicted cardiovascular events independently of guideline-recommended clinical risk factors alone (18).

    In a cohort of 1,030 subjects with type 2 diabetes with or without previous CVD, we also found albuminuria to be related to echocardiographic abnormalities (19). When this cohort was followed for 4.8 years, a range of echocardiographic parameters predicted CVD in this cohort; however, in multivariable analyses, mean E/e′ (a measure of diastolic dysfunction) was the strongest predictor and had the highest model performance. We observed a hitherto undescribed sex interaction, as mean E/e′ performed best in men, whereas in women GLS was best (20).

    Markers From Different Pathways Predict Heart and Kidney Outcomes

    As an alternative description of the cardio-renal syndrome, Zannad and Rossignol described risk factors such as diabetes and hypertension, activating pathways such as inflammation, oxidative stress leading to fibrosis, and inflammation affecting both the kidney and heart (21). This model can be used for precision medicine in using biomarkers related to the different activated pathways to guide therapy (Fig. 3). After many years with renin-angiotensin system (RAS) blocking agents as the only therapy for DKD, we are currently in the fortunate situation of having a number of potential therapies for DKD that have been or are being evaluated in phase 3 studies with cardiovascular or renal primary end points. Combination therapy including all agents is probably neither feasible nor safe, and assuming pathophysiological heterogeneity between people with DKD, application of therapies based on relevant biomarkers may thus be a way forward to optimize benefit and minimize adverse events.

    Figure 3
    Figure 3

    Potential risk factors, pathological pathways, and corresponding markers on the path to heart and kidney complications. B-Glucose, blood glucose; BNP, brain natriuretic peptide; U-CKD273, urinary proteomic marker of chronic kidney disease; u-CAD238, urinary proteomic marker of coronary heart disease; proC6, serum PRO-C6 (marker of fibrosis); 8-oxodG, 8-oxo-7,8-dihydro-2′-deoxyguanosine (see text for details).

    Vascular Damage

    As discussed initially, elevated urinary albumin excretion reflects widespread vascular damage and predicts development of renal failure and cardiovascular events. In addition, treatment-induced reductions are associated with improved renal and cardiac prognosis as initially demonstrated in smaller studies (22,23) and recently documented in meta-analyses of observational (24) and intervention (25) studies. Thus, albuminuria has been an inclusion criterion in most renal outcome studies in diabetes and a surrogate outcome in many phase 2 studies. For several decades, elevated albuminuria has been clinically used as an indicator for cardioprotective therapy with RAS-blocking agents.

    Troponin T has, in addition to its use in acute settings as a marker of myocardial damage, been used to demonstrate vascular, cardiac, and renal risk in both type 1 and type 2 diabetes and could be a marker of increased risk for atherosclerosis (26,27). Trimethylamine-N-oxide (TMAO), is a metabolite of phosphatidylcholine, choline, and carnitine produced by the gut microbiota from ingested animal food sources (meat, eggs, and fish). A higher level of TMAO has been suggested as an independent risk factor for renal impairment and CVD. First, simply as a biomarker of recurrent CVD in people with known CVD (28), but TMAO might be mechanistically involved in the pathogenesis of CVD, as it has been shown to be associated with higher levels of cholesterol in macrophages and it has been shown to enhance the risk of thrombosis by promoting platelet hyperactivity. We demonstrated that higher TMAO was associated with renal and cardiac events during follow-up in type 1 diabetes (29), although not independently of renal function, maybe because it is a marker of filtration or because the effect is mediated by impaired renal function. In type 2 diabetes, it was also predictive of cardiovascular damage (30).

    Fibrosis

    We studied, as a marker of fibrosis, serum and urine PRO-C6, a product specifically generated during collagen VI formation. We tested whether it is prognostic for adverse outcomes in individuals with type 2 diabetes and microalbuminuria. We found a doubling of serum PRO-C6 increased hazards for cardiovascular events (hazard ratio [HR] 3.06 [95% CI 1.31–7.14]) and all-cause mortality (6.91 [2.96–16.11]) and reduction of estimated GFR (eGFR) of >30% (4.81 [1.92–12.01]) (see Fig. 4). We also tested this in type 1 diabetes and found similar results (31), although in individuals with type 1 diabetes the association with cardiovascular events was lost after adjustment for other risk factors.

    Figure 4
    Figure 4

    Serum PRO-C6 (marker of fibrosis) associated with kidney disease progression (defined as a decline of eGFR of >30% from baseline) (A) and cardiovascular events (cardiovascular mortality, stroke, ischemic CVD, and heart failure) (B) in subjects with type 2 diabetes (n = 200) (60). Dotted line, tertile 1 (T1); dashed line, tertile 2 (T2); solid line, tertile 3 (T3).

    Applying urinary proteomic analysis with capillary electrophoresis coupled to mass spectrometry, Good et al. (32) described a high dimensional urinary biomarker pattern composed of 273 peptides associated with overt kidney disease: CKD273. The original studies included people with chronic kidney disease on a mixed background compared with healthy control subjects. The components of CKD273 include collagen fragments and are assumed to relate to early fibrosis in the kidney. In retrospective studies, this proteomic classifier identified subjects at risk for DKD and progression in albuminuria class earlier than the indices currently used in clinical practice (33). We tested, in a prospective study including people with type 2 diabetes and normoalbuminuria, whether CKD273 was associated with development of microalbuminuria and whether progression to microalbuminuria could be prevented with the mineralocorticoid receptor antagonist (MRA) spironolactone (34) (see Fig. 5). We chose spironolactone, as this MRA had been proposed to prevent fibrosis and had been demonstrated to reduce albuminuria in DKD (35). We followed 1,775 participants; 12% (n = 216) had a high-risk urinary proteomic pattern, of whom 209 were included in the trial and assigned spironolactone (n = 102) or placebo (n = 107). Median follow-up time was 2.51 years. Progression to microalbuminuria was seen in 28.2% of high-risk and 8.9% of low-risk participants (P < 0.001) (HR 2.48 [95% CI 1.80–3.42], P < 0.001). There was no significant effect of spironolactone on development of microalbuminuria (HR 0.81 [95% CI 0.49–1.34] P = 0.41), which may reflect lack of power, or alternatively it only works in established chronic kidney disease. Based on the same urinary proteomic technology, different signatures associated with heart failure (HF1) (36) or atherosclerotic CVD (CAD238) (37) have been developed but less thoroughly evaluated.

    Figure 5
    Figure 5

    Design of the PRIORITY study, testing a urinary proteomic biomarker, CKD273, of risk for DKD and the potential for mitigating risk for progression to microalbuminuria in normoalbuminuric subjects with type 2 diabetes with spironolactone (34).

    Inflammation

    Multiple markers have been investigated related to inflammation. These include fibrinogen, interleukin 6, and TNFα, which were found to be associated with risk of chronic kidney disease progression (38). Some of the most widely studied markers have been tumor necrosis factor receptor (TNFR)1 and 2. Recently, the Kidney Risk Inflammatory Signature (KRIS) was developed with 17 inflammatory markers including TNF receptor superfamily members (39). The signature was tested in two cohorts as a marker of end-stage kidney disease in both type 1 and type 2 diabetes. All components of the signature had a systemic, nonkidney source and may guide therapy to new targets. Interestingly, the signature was improved with the anti-inflammatory agent baricitinib but not with RAS blockade (39).

    Soluble urokinase plasminogen activator receptor (suPAR) is considered an important inflammatory marker implicated in endothelial and podocyte dysfunction. We tested suPAR in type 1 diabetes and found it to be an independent risk marker of cardiovascular events, kidney function decline, and mortality. We observed an adjusted HR per doubling of suPAR for cardiovascular events (n = 94), progression in albuminuria (n = 36), eGFR decline (n = 93), end-stage kidney disease (n = 23), and mortality (n = 58) of 3.13 (95% CI 1.96–5.45), 1.27 (0.51–3.19), 2.93 (1.68–5.11), 2.82 (0.73–11.9), and 4.13 (1.96–8.69), respectively.

    Oxidative Stress

    It has been proposed that elevated levels of uric acid induce vascular and kidney damage, hypertension, and atherosclerosis due to inflammation and oxidative stress. We, and others, demonstrated elevated uric acid levels to be associated with cardiovascular events and progression of renal disease in type 1 diabetes (40). In the Prevention of Early RenaL function loss study (PERL), we tested whether lowering of uric acid with allopurinol in people with type 1 diabetes and early DKD with albuminuria or declining eGFR could prevent loss of measured GFR over 3 years. Mean serum urate level decreased from 6.1 to 3.9 mg/dL with allopurinol and remained at 6.1 mg/dL with placebo. Despite this, we found no evidence of a kidney-protective effect on albuminuria or decline in GFR (41). Although this suggests uric acid is not a target, in line with a Mendelian randomization study in type 1 diabetes (42), a study was presented in 2019 with larger reduction of uric acid in a small group of individuals with type 2 diabetes followed for 24 weeks with a urate reabsorption inhibitor, verinurad, and feboxustat in combination, giving a 49% reduction in urine albumin-to-creatinine ratio compared with placebo (43).

    Other markers of oxidative stress are oxidatively modified guanine nucleosides 8-oxo-7,8-dihydro-2′-deoxyguanosine and 8-oxo-7,8-dihydroguanosine (8-oxoGuo) excreted in the urine. The level of 8-oxoGuo was associated with mortality and CVD in type 2 diabetes (44).

    For clarification of whether the different markers from the diverse pathways are useful to guide selection of therapy, post hoc analyses of randomized controlled studies are useful, but ideally, there is a need for prospective studies designed to test the hypothesis that biomarker-guided therapy is better than standard of care. We have started investigating whether subjects with type 1 and type 2 diabetes have different responses to different interventions and whether these differences can be predicted by the biomarkers. Thus, participants are in random order receiving four different treatments targeting different pathways to test response and association with biomarkers before treatment.

    New Treatment Options for Cardio-Renal Complications in Diabetes and Ideas for Personalized Selection of Agents

    For more than 20 years, standard of care in people with diabetes and kidney disease has included treatment with RAS-blocking agents, either ACE inhibitors or angiotensin receptor blockers, in addition to control of lifestyle factors, blood glucose, lipids, and blood pressure (45). Thus, selecting treatment to protect the kidney was not complicated. Although this improved prognosis for people with DKD, there was a large unmet need. The effect on renal end points was significant but modest (HR 0.80), and for the heart there was benefit of controlling blood pressure and reducing heart failure, but RAS blockade did not provide benefit on mortality or CVD in these studies. New agents either increasing blockade of RAS or targeting other pathogenetic pathways were needed. Many strategies have been tested and failed during the past 20 years either due to side effects or due to lack of effects, such as ACE inhibitors plus angiotensin receptor blockers, renin inhibition, erythropoetin, avosentan, and bardoxolone. During the past couple of years, we have seen significant progress, with new agents showing benefit on renal and/or CVD end points in people with type 2 diabetes and chronic kidney disease. For most tested agents, the effects on heart and kidney have been linked but in different ways. For some, there were benefits on the kidney but side effects like heart failure; for others, there were benefits on kidney and heart. Although not all agents are on the market yet, we need to find out how to choose the best agent, or combination of agents, for an individual to provide optimal benefit for heart and kidney and minimal risk for side effects. We believe that the discussed physiological tests and biomarkers may be helpful in selecting between agents, although it should be stressed that this remains to be tested.

    SGLT2 Inhibitors

    The first, and so far, most marked, success has been with SGLT2 inhibitors, initially tested for safety in cardiovascular outcome trials, where not only a benefit on the primary end point major adverse cardiovascular events was demonstrated with empagliflozin (HR 0.86 [95% CI 0.74–0.99], P = 0.04 for superiority) (46). A significant benefit on hospitalization for heart failure was also observed. In addition, a reduction in incident or worsening nephropathy occurred (HR 0.61 [95% CI 0.53–0.70]) (47). These findings were confirmed in cardiovascular outcome trials with canagliflozin and dapagliflozin. The first study with hard renal end points (end-stage kidney disease, significant loss of renal function) as the primary end point using a SGLT2 inhibitor was Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE), showing a major benefit not only on renal outcome but also on heart failure and major adverse cardiovascular events in people with type 2 diabetes (urine albumin-to-creatinine ratio >300 mg/g and eGFR 30–90 mL/min/1.73 m2) (48). The primary outcome was a composite of end-stage kidney disease, a doubling of the serum creatinine level, or death from renal or cardiovascular causes. The study was stopped early showing a benefit of canagliflozin with HR 0.70 (95% CI 0.59–0.82). These data were confirmed and extended by Dapa-CKD (A Study to Evaluate the Effect of Dapagliflozin on Renal Outcomes and Cardiovascular Mortality in Patients With Chronic Kidney Disease) including subjects with chronic kidney disease with or without diabetes (49). Whereas SGLT2 inhibitors were introduced to treat hyperglycemia, they also provide organ protection in individuals without diabetes with heart failure and/or chronic kidney disease. The explanation for the renal and cardiac benefits is not clear but may involve interaction between the organs (50). Recently, neuropathy and renal innervation were implicated (51). It is now recommended that they be added to standard of care in type 2 diabetes with chronic kidney disease (52), and in addition to patients with albuminuria and eGFR criteria, patients at risk for or with heart failure would potentially benefit the most (Fig. 6).

    Figure 6
    Figure 6

    Biomarker-guided treatment selection. A proposal for how biomarkers could guide selection of treatment among recently tested options with a precision medicine approach in diabetic kidney and heart disease (“Complication” in inner circle). Using available “Supporting Biomarkers” (green circle) reflecting underlying pathology and “Risk Biomarkers” or contraindications (red circle) to select optimal treatment (outer circle) in patients with type 2 diabetes. Thus, as an example in CKD: elevated urinary albumin-to-creatinine ratio (UACR) or fluid retention (brain natriuretic peptide [BNP]) would suggest an SGLT2 inhibitor (SGLT2i), whereas markers of inflammation and fibrosis would suggest nonsteroidal MRA (nsMRA) (currently not available), and suPAR would suggest endothelin receptor 1A antagonist (ET1Aant) (currently not available) unless there are signs of fluid retention (elevated NTproBNP). Aldo, aldosterone; ASCVD, atherosclerotic CVD; HF, heart failure; CKD, chronic kidney disease; Echo, echocardiography; CACS, coronary artery calcium score; K+, potassium; U-CKD273, urinary proteomic marker of chronic kidney disease; u-CAD238, urinary proteomic marker of coronary heart disease; HF1, urinary proteomic marker of heart failure; proC6, serum PRO-C6 (marker of fibrosis); TNT, troponin T; suPAR, soluble urokinase plasminogen activator receptor.

    Atrasentan

    The Study Of diabetic Nephropathy with AtRasentan (SONAR) was presented simultaneous with the presentation of CREDENCE (53). Although stopped early for concern of futility, the study eventually showed a renal benefit of the same magnitude as in CREDENCE, but with no effect on major adverse cardiovascular events and a tendency to increased risk of heart failure, which also stopped another ET1A receptor antagonist, avosentan. The mode of action may relate to an effect on inflammation, but also an effect on podocytes and glycocalyx has been proposed from experimental data (54). Thus, we propose that suPAR is used to identify subjects who would benefit, and markers of heart failure would exclude the use of atrasentan (Fig. 6).

    GLP-1RA

    For some of the long-acting GLP-1RA (liraglutide, semaglutide, dulaglutide), the cardiovascular outcome trials in type 2 diabetes demonstrated cardiovascular benefits in subjects with already existing atherosclerotic CVD (52). There were renal benefits as secondary end points, mostly driven by reductions in albuminuria, but also some potential effects on eGFR. This was supported by the AWARD-7 study with dulaglutide in individuals with DKD, although the primary end point was glycemic control (55). It remains to be demonstrated whether there will be benefits on hard renal end points in addition to cardiovascular benefits; this is currently being tested in the FLOW study (clinical trial reg. no. NCT03819153, ClinicalTrials.gov). It is suggested that albuminuria and BMI as well as markers related to vascular damage, including troponin T, CAD238, TMAO, and elevated coronary calcium score on CT imaging (or 82Rb PET/CT), could be used to identify relevant subjects, and as there is no impact on heart failure, heart failure was used as exclusion criteria (Fig. 6). Currently we are involved in investigations of the mode of action of the effect on atherosclerosis, and the study may provide insight into more specific markers or imaging techniques to guide therapy (clinical trial reg. no. NCT04032197, ClinicalTrials.gov).

    Mineralocorticoid Receptor Antagonism

    Short-term studies revealed reduction in proteinuria in DKD with the steroidal MRAs spironolactone and eplerenone (35)—an interesting strategy, as preventing overactivation of the mineralocorticoid receptor reduces inflammation and fibrosis, but due to potassium problems, diabetes and kidney disease became a contraindication for these agents. Nonsteroidal MRAs have been developed and may have the anti-inflammatory and antifibrotic effects with less potassium problems. Esaxerenone and finerenone were demonstrated to reduce microalbuminuria in type 2 diabetes (56,57). Two phase 3 trials with finerenone was started in type 2 diabetes with chronic kidney disease, and the first has been stopped and it has been announced that the primary renal and secondary cardiac outcomes were positive but not yet presented. Preclinical studies demonstrated improved effect on inflammation and fibrosis in the heart (58) and kidney (59), and thus depending on the data, nonsteroidal MRAs like finerenone may be preferred when inflammation (KRIS, TMAO) and fibrosis (CKD273, serum PRO-C6 [marker of fibrosis]) and perhaps aldosterone are elevated, whereas it remains to be seen whether potassium will be an issue (Fig. 6).

    Conclusions

    In diabetes, the heart and kidney are now doing better, thanks to recent advances in diagnosis and therapy. The next step is to convert this into fully individualized medicine, combining new possibilities in imaging and biomarker-based risk prediction with detailed knowledge of therapeutic avenues. This will ensure optimal treatment and prevent adverse events and unnecessary polypharmacy. A more detailed approach when choosing the right treatment for the right person may seem complicated and costly at first but has the potential to save both patients and the health care system considerable costs.

    The amount of information supporting design of individualized treatment is expected to grow drastically soon. Studies of the kidney and the heart using functional MRI and kidney biopsy studies will lead to a better diagnostic discrimination. At the same time, genomics, epigenomics, and metabolomics studies increase our knowledge of physiological processes. All of this will increase the complexity of the diseases but holds promise for better understanding once we learn to interpret the large amount of data available. Hopefully, this will lead to a better prevention of renal and cardiovascular outcome in the future.

    Article Information

    Funding. The authors were supported by the Novo Nordisk Foundation grant PROTON – PeRsOnalizing Treatment Of diabetic Nephropathy (NNF14OC0013659).

    Duality of Interest. P.R. has received honoraria to Steno Diabetes Center Copenhagen from teaching and consultancy for Astellas, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, Gilead, Novo Nordisk, Merck, Merck Sharp & Dohme (MSD), Mundipharma, Sanofi, and Vifor. F.P. has served as a consultant on advisory boards or as an educator for AstraZeneca, Novo Nordisk, Sanofi, Mundipharma, MSD, Boehringer Ingelheim, Novartis, and Amgen and has received research grants to his institution from Novo Nordisk, Amgen, and AstraZeneca. No other potential conflicts of interest relevant to this article were reported.



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