#Diabetic Gastroparesis Symptoms

[diabetesreversalprograminindia]

Type 2 Diabetic Gastroparesis: Causes, Symptoms, Treatment

This article is originally published on Freedom from Diabetes website, available here. Are you living with Type 2 Diabetes and struggling with poor digestion? Do you want to know the reason behind this. Gastroparesis may be the culprit. This condition affects millions of individuals worldwide, causing delayed stomach emptying and a range of uncomfortable symptoms. You have to take proper guidance from your doctor.

Also here, we will discuss about Type 2 Diabetic Gastroparesis and their causes, risk factors, diagnosis and treatment options. So let's get started on the journey towards better digestive health! First understand what is Type 2 Diabetic Gastroparesis?

What is Type 2 Diabetic Gastroparesis?

Type 2 diabetes is a chronic condition that affects the way your body metabolizes glucose (sugar). Glucose is the body’s main source of energy and comes from the food you eat.

Insulin, a hormone produced by the pancreas, helps cells use glucose for energy. In type 2 diabetes, either your body doesn’t produce enough insulin or the cells don’t respond properly to insulin, causing a buildup of sugar in your bloodstream. Type 2 diabetes can also cause gastroparesis, a condition in which your stomach muscles stop working properly and food moves too slowly through your digestive system. Gastroparesis can make it difficult to control blood sugar levels. Lets understand the symtoms of gastroparesis include nausea, vomiting, bloating, abdominal pain, and weight loss. If you have any of these symptoms, see to your a doctor.

Causes of Type 2 Diabetic Gastroparesis?

The precise cause of type 2 diabetic gastroparesis is unknown, but it is thought to be due to a combination of factors. First, type 2 diabetes itself can damage the nerves that control the muscles of the stomach (the vagus nerve), which can lead to gastroparesis. In addition, some medications used to treat type 2 diabetes (such as metformin) can also cause or contribute to gastroparesis.

How Is Type 2 Diabetic gastroparesis Diagnosed?

A medical history and physical examination. This can help your doctor rule out other possible causes of your symptoms, such as ulcers or dumping syndrome.

A small tube will be inserted through your nose into your stomach. You will then be given a radioisotope-tagged meal to eat. The amount of radioactivity in your stomach will be measured over the next few hours to determine how quickly your stomach is emptying.

An upper GI endoscopy.

A gastric emptying breath test.

You have to remember these things for sure while managing and treating type 2 diabetic gastroparesis, it’s important to keep your blood sugar levels under control. This can be done by following a healthy diet, maintaining a regular exercise routine, and monitoring your blood sugar levels regularly. Also taking the peoper medication as prescribed and should not skipping doses. Be more careful about the side effects of your medication and report them to your doctor right away.

Diet and Lifestyle Tips for Type 2 Diabetic Gastroparesis

Avoid large meal, eat small, frequent meals and snacks.

Go for low-fat and easy-to-digest foods.

Limit high-fiber foods, as they can slow digestion.

Avoid spicy foods, as they can irritate the stomach.

Stay hydrated by drinking plenty of fluids throughout the day, including water, clear juices, and decaffeinated tea or coffee. Limit alcoholic beverages.

That's all about the diabetic gastroparesis. Keep your health on priority, follow these instructions, tips properly. If you want to know more about gastroparesis, please visit our Article. Also please connect with me on my website, Facebook page, and YouTube if you want to stay in touch or give me any feedback!

[diabetes-health-corner]

Type 2 Diabetic Gastroparesis

Type 2 diabetes is a chronic condition that affects the way your body metabolizes glucose (sugar). Insulin, a hormone produced by the pancreas, helps cells use glucose for energy. The symptoms of gastroparesis include nausea, vomiting, bloating, abdominal pain, and weight loss.

Click here to read more: https://www.freedomfromdiabetes.org/blog/post/type-2-diabetic-gastroparesis-causes-symptoms-and-treatment/3496

[usascripthelpersofficial]

🌀 Diabetic gastroparesis is a condition where the stomach takes too long to empty its contents, often due to nerve damage from diabetes.

🚨 Symptoms to Watch For:

Nausea or vomiting

Feeling full early

Abdominal bloating

Lack of appetite

💡 Treatments Include:

Dietary changes

Medications like metoclopramide

In severe cases, devices to stimulate stomach muscles

👨‍⚕️ Always consult your healthcare provider for a diagnosis and tailored treatment plan. Stay informed and take control of your health!

[cannabiscomrade]

It's Gastroparesis Awareness Month

Hi! I have gastroparesis and I'm an insufferable know-it-all so let's talk about it!

Gastroparesis, or a paralyzed stomach, is a condition that causes delayed gastric emptying.

This can cause a range of symptoms and complications:

nausea

vomiting

early satiety/fullness

upper gastric pain

heartburn

malabsorption

dehydration

malnutrition

Gastroparesis can be treated by a gastroenterologist, but often needs to be managed by a motility specialist due to a lot of misconceptions about the condition. Providers, especially in the emergency department, will commonly misdiagnose gastroparesis as cannabis-hyperemesis syndome, cyclic vomiting syndrome, gastritis, food poisoning, etc.

There are several commonly known causes of gastroparesis like vagus nerve damage from diabetes, injury to the stomach, and stomach surgery like hernia repair or bariatric surgery. There are also idiopathic cases with no known cause. Other causes of gastroparesis are:

Connective tissue disorders like HSD and EDS (commonly hEDS and cEDS)

Post-viral (like COVID, viral gastritis, mononucleosis/Epstein-Barr)

Restrictive eating disorders

Autoimmune diseases like Systemic sclerosis (scleroderma), Lupus, Hashimoto's

Central nervous system disorders

Gastroparesis also has common comorbidities with conditions like:

POTS and other forms of dysautonomia (POTS, EDS, and gastroparesis are a common triad of diagnoses)

MCAS

SMAS (which can also present with similar symptoms to GP)

Intestinal dysmotility and esophageal dysmotility disorders (known as global dysmotility)

PCOS with insulin resistance

Endometriosis

SIBO/SIFO

Chronic intestinal pseudo-obstruction

Migraines

Certain medications like Ozempic and other drugs in that class act on the digestive system to delay gastric emptying, which has caused people to be diagnosed with gastroparesis. Some people report that their cases have not gone away since stopping the medication, others report feeling better after stopping. Other drugs like opiates and narcotics can cause delayed gastric and intestinal motility as well, but these are commonly known side effects of those painkiller classes.

Gastroparesis is classed based on severity and graded based on how you respond to treatment.

Severity of delay ranges from mild to very severe, and this is based on your actual stomach retention calculated at 4 hours into a gastric emptying study.

The grading scale ranges from one to three, one being mild and three being gastric failure.

There is no consistent single treatment that is proven to work for gastroparesis, and there is no cure. Treatments can consist of:

Diet changes (3 Step Gastroparesis Diet, liquid diet, oral sole source nutrition)

Prokinetic (motility stimulating) drugs

Anti-nausea medications

Proton-pump inhibitors

Gastric stimulator/gastric pacemaker

Pyloric botox and dilation

G-POEM/pyloroplasty

Post-pyloric tube feeding

Gastric venting/draining

Parenteral nutrition

IV fluids

Other surgical interventions like gastrectomy or rarely, transplant

Gastroparesis is a terrible disease and I hope that if any of these symptoms resonate with you that you can get checked out. I was misdiagnosed for a long time before getting a proper gastroparesis diagnosis, and all it took was a gastric emptying study. This is ESPECIALLY true if you're having post-COVID gastrointestinal problems that are not improving. I almost died from starvation ketoacidosis because of how serious my GP got in a short period of time post-COVID (I had GP before COVID), and now I'm tube reliant for all my nutrition and hydration.

Stay safe friends!

[3liza]

Saw your post asking about insulin resistance without high blood sugar, and yeah I have experience with that exact thing. Everyone in my family has some sort of awful blood sugar issues, but despite having something clearly wrong with me my glucose tests and a1c's were coming back thoroughly normal. I got lucky with a decent doctor and she ordered an insulin test (usually more accurate with fasting I believe, but the result was rather high anyways) and she noted that it was high and told me to try out a diabetes diet to see if it helped.

I'm on a strict low-glycemic index diet now and it's really improved my health, mostly my mental health, but my skin has been upgraded from "abysmal" to a firm "mediocre."

Do I know what's wrong? No. Probably never will, but I'm feeling a lot better at least.

huh. thats useful info. im about to get a new doctor, i wonder if she'll be willing to entertain this sort of weirdness

edit: i just feel Bad and Sick if i eat a sufficient amount of sugar. systemic symptoms, skin gets worse, actual skin pathology like wounds not healing or eczema/psoriasis/fungus gets worse, migraines get triggered, pain flares, etc. not normal person "i ate too much sugar i feel temporarily sub-optimal" halloween candy coma, but i will get actually sick for a few days if i over-indulge. but i crave sugar constantly, which doesnt really mean anything, lots of people crave sugar because It Tastes Good so its not exactly diagnostic. sometimes the sugar cravings seem uncontrollable, like "i need to get out of bed where i am trying to sleep and eat something sweet or i cant think about aything else" kind of stuff. my parents do this same dance with carbohydrates and sugar, they feel awful, eat a cookie, feel awful, recover, say stuff like "oh i shouldnt eat the cookie", and it cycles. some of it is eating disorder crap, which is real hard to differentiate from other issues. some of it is being underweight/underfed from gastroparesis (which I have, pretty badly) which means certain circumstances of calorie shortages, bad digestion, whatever, can align perfectly to trigger I Am Starving I Need to Overeat Right Now Or I'll Die programming in the ape brain, and again, thats real hard to separate from blood sugar symptoms and eating disorder symptoms because they all get tied up together.

however, if i manage to grocery shop in the correct way to provide myself with ample available appropriate food, and i can eat ketogenic or nearly-ketogenic with focuses on dairy fat and just regular animal meat and fresh veg, with minimal or no grains, starches, and sugars, i feel like 60% better on all axes. my dad, too, eventually, after he got diagnosed, was instructed to stop eating most carbs etc and immediately lost all the extra weight he was uncomfortable with his whole life, and immediately got less chronically crappy-feeling. so there's something going on, i just dont know if its medical or genetic or what. some people just dont do well with a lot of grains and theres no particular medical reason.

[sebs-out-of-spoons]

🌕 Introduction Post 🌕

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Hi there, fellow spoonie! I’m Sebastian, and this is my blog for my diagnosis journey. Welcome! <3

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Things To Be Diagnosed

Physical

hEDS (Hypermobile Ehlers-Danlos Syndrome) or HSD (Hypermobile Spectrum Disorder)

POTS (Postural Orthostatic Tachycardia Syndrome)

Diabetes or Hyperglycemia or Hypoglycemia (We aren’t sure yet)

?Gastroparesis? (Still very unsure)

Mental

ASD (Autism Spectrum Disorder)

ADHD (Attention Deficit Hyperactive Disorder) (Combined Type)

C-PTSD (Complex Post-Traumatic Stress Disorder) or PTSD (Post-Traumatic Stress Disorder)

Pure O OCD (“Purely Obsessional” Obsessive-Compulsive Disorder)

SPD (Sensory Processing Disorder)

APD (Auditory Processing Disorder)

ARFID (Avoidant/Restrictive Food Intake Disorder)

SAD (Social Anxiety Disorder) BDD (Body Dysmorphic Disorder)

Trichotillomania

Dermatillomania

Overlapping

PMDD (Premenstrual Dysphoric Disorder)

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Already Diagnosed

MDD (Major Depressive Disorder)

GAD (Generalized Anxiety Disorder)

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About This Blog

I’ll probably mainly be posting about the progress on my physical diagnoses. I will be posting about PT, my chronic pain, dislocations and subluxations, pre-syncope, and everything to do with my physical symptoms and struggles.

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More Things

I have an appointment with a Physical Therapist on Tuesday, 9/24/2024. I will be working with them for my chronic joint pain caused by my hypermobility and my low exercise endurance/tolerance (likely caused by suspected POTS).

I have an appointment with a cardiologist on 11/4/2024 to figure out and diagnose my POTS and maybe they can figure out and diagnose my hEDS or HSD as well (if I just miss the criteria for hEDS, then it’s probably HSD, but I’m pretty sure it’s hEDS). We aren’t sure who can figure out and diagnose that yet, but we’re looking into resources. (I also have an appointment that same day with a gender clinic to see if I can get some of/all of my neurodivergencies diagnosed.)

I went for bloodwork today (9/20/2024), and they’ll be testing for multiple things, including diabetes, hyperglycemia, and hypoglycemia. I’ll have results around 9/23/2024.

I have been showing symptoms of hEDS/HSD since I was 7-years-old (dislocations & subluxations, soreness & stiffness, severe “growing pains”, pain, mild skin hyperextensibility, chronic headaches, etc.), and symptoms of POTS alongside that since I was around 10-years-old.

I suffer from chronic pain, chronic dislocations & subluxations, chronic stomach issues, hypermobility (about an 8/9 on the Beighton Scale), (?chronic?) fatigue, and more stuff.

After being diagnosed, I am hoping to get mobility aids (cane, arm crutches, possibly a wheelchair one day if things get bad enough or for on the really bad days), joint braces, compression socks, and more to help with these things.

I am also celiac, have a dairy allergy, have environmental allergies, like dust, mold, and pollen.

I struggle with my eating due to my undiagnosed ARFID, POTS, and possible Gastroparesis. So, beware, I am always incredibly mood swingy due to that.

Daily Pain Scale

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About Me

I’m a Queer, Nonhuman, Neurodivergent, and Disabled Transman.

I’m 16-years-old, and will be turning 17-years-old this year (2024).

I have a job as a busser that I go to once a week due to my low tolerance to sensory input and exercise.

I am taken by my amazing boyfriend, @insidedarcysdiary (He/It/Ze/Xe).

I have one sibling (He/She), who I won’t be tagging since he isn’t on here much.

My Special Interests are: Wings Of Fire, Harry Potter (fuck the author, I’m mainly here for the dead gay wizards), Dragons, and currently my most active special interest is Neurodivergency & Disabilities.

My Current Hyperfixation is: Neurodivergency & Disabilities, specifically my own.

I’m queer in many ways: Trans (FTM), Genderqueer, Enby (and under the umbrella), Xenogender, AroAce (+ Onealterous, Onequeerplatonic, Oneexteramo, Pansensual, Panaesthetic, Panplatonic), Ambiamorous, T4T-leaning, and Lesboy.

I’m nonhuman in many ways as well: Polytherian, Polykin, Otherfix, Otherhearted, Otherflicker/Fictionflicker, Transspecies (radqueer fuck off), Humanfluid, Pseudohuman, Physical Nonhuman, and Voidpunk.

I love drawing, creating things, reading, and writing. Mainly, my hyperfixations and special interests take over my life, so I don’t have the energy or time for anything else (and then sometimes, my possible chronic illnesses take over my hyperfixations and special interests, and I’m not even able to muster energy to do them).

Tone tags/indicators are incredibly helpful for me, PLEASE USE THEM!

If you have any questions about anything, please ask me and I will not be bothered.

I don’t have the energy to make a DNI list, but just know that I will block you loads if you do fall under my mental DNI list.

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[cartoonscientist]

it’s kind of interesting how there’s that truism that people shame mental illness and don’t take it seriously whereas they accept physical illness as valid, which is true on a generalized scale, but also… we kind of do shame and minimize physical illnesss

in the 80s, it was “only NERDS have allergies or asthma”, in the 90s it was “diabetes is caused by being hooked up to a McDonald’s shake IV for ten years!”, now it’s “oh, you have IBS? right. I bet you’re one of those entitled chronic illness tiktok fakers, IBS technically isn’t a real illness” “I don’t trust any women who claim to have gastroparesis” “you wouldn’t have been hit by a car if you had been paying attention and heard it speeding through the crosswalk, the right of way doesn’t mean you’re invincible” “you gave YOURSELF lung cancer, you’re lying about not smoking” or even “pinkeye is caused by rubbing poop in your eye dude, you must not wash your hands”

people who have been proven to have a malformed sphincter in their esophagus are having their throats scarred and burnt by stomach acid because doctors refuse to believe that GERD is caused by anything but obesity and poor dietary habits

also there’s just like a whole arcane list of symptoms that will make doctors and nurses treat you like a criminal

[hexen-cosplay]

Health Problems & Cosplay

I mentioned in a previous post that I am a cosplayer with health conditions, and in this post I’m going to talk about them a little bit! Now, you may have noticed that I said ‘them’, and that’s because I have collected quite a few of them over the years and here they are:

🖤 TYPE 1 DIABETES 🖤

The pancreas stops producing the hormone insulin, and as such to keep blood glucose levels from rising and causing a fatal complication known as Diabetic Ketoacidosis, T1 Diabetics must take insulin every single day to stay alive. 

🖤 GASTROPARESIS 🖤

Gastro = “stomach”. Paresis = “partial paralysis”.

The basics of this disease, is that food does not pass through my stomach at the speed it should. It goes a lot slower, and this causes a multitude of often debilitating symptoms, including: intense bloating, not being able to eat enough food resulting in deficiencies and malnutrition, extreme stomach pain, constant nausea, vomiting a lot (sometimes undigested food), constipation/diarrhoea, reflux, and more. 

🖤 SINUS TACHYCARDIA/POTS 🖤

Sinus tachycardia is a regular cardiac rhythm in which the heart beats faster than normal. The PoTS is suspected due to experiencing black outs (which once resulted in two broken ribs), extreme dizziness, blurred vision, chest pain, shortness of breath and changes in blood pressure. 

🖤 AUTONOMIC NEUROPATHY 🖤

Autonomic neuropathy occurs when there is damage to the nerves that control automatic body functions - the things we don’t think about every day, that happen automatically. It can affect blood pressure, temperature control, digestion, bladder function and even sexual function.

🖤 PROLIFERATIVE DIABETIC RETINOPATHY & MACULAR OEDEMA 🖤

This is the last and most serious stage of Diabetic Retinopathy. In the first two stages, the changes are reversible. In stage 3 new blood vessels and scar tissue have formed on your retina, which can cause significant bleeding (you can see the bleeds in your vision, which is distressing and causes impairment), and lead to retinal detachment, where the retina pulls away from the back of the eye. At this stage, there's a very high risk of blindness.

HEALTH PROBLEMS & COSPLAY

As you may have guessed, this is a lot! It’s a lot to deal with, I’m in pain all the time, and it makes me quite grumpy sometimes too. 

My ongoing health struggles did play a part in the break I took from cosplaying, but that break turned into almost 9 years. It wound up that way because I convinced myself that I had to wait until I felt better to start again so that I could wholly dedicate myself to it. That was not a good mindset for me because I was still dealing with some denial over my health, despite knowing deep down that I would never "get better" in the way that I wanted to. My conditions are chronic. They're never going away.

I've come a long way in the 8 and a bit years since my last cosplay, though, and I'm not in denial anymore about my wellness. I take my medications, and I go to check-ups; I do the things that I need to do to make my life easier and ultimately, keep me alive. I know that sounds like a bare minimum, but it's not always that easy when your head is in a gnarly space, like mine was.

Alongside the.. peronal overhaul, I've employed a lot of new strategies in my day-to-day life that allow me to be myself and do the thing that I love, because I really do love cosplaying! By pacing myself, resting when I need to and not telling myself that needing it is failing, I'm kinder to myself - this kindness in place of self-deprecation for not being fast enough or as quick as another cosplayer has been the biggest turning point. I stopped comparing myself to people that didn't have to face what I do; I took a step back and took time to come to terms with the fact that I am different, and as such, I need to look at and do things differently, to suit my lifestyle and the things I have to content with. That took a lot of courage to do, despite it being a very introspective process, because facing yourself like that is hard. In my own mind, my differences made me lesser for many years, and it took actively challenging that perception within myself to realise that I was making my life harder, and denying myself happiness and fulfilment because of it.

Nowadays, I congratulate myself on progress because I am worth praise and worth happiness; I no longer view asking for help as a weakness or a failure, and I don't compare my progress to that of others. I acknowledge and accept that my conditions and disability exist, do not make me lesser, and require alternative means of doing things. Needing these accommodations and adaptations doesn't make me less as a person, or less worthy of love, happiness, praise and fulfilment than anyone else, not only in cosplay but life in general.

PATREON | TIKTOK | DEVIANTART | INSTAGRAM | REDDIT | FACEBOOK | TWITTER | YOUTUBE | TWITCH

[fursasaida]

fucking hell. turns out ozempic/wegovy/etc is giving people gastroparesis. they are saying "extreme cases" are rare so far. who knows what the definition of "extreme" is. and at this point in my life I am automatically skeptical of declarations that medical conditions are rare. to wit:

In clinical trials, nearly half of people, 44%, who took Wegovy reported nausea, and almost 1 in 4 reported vomiting; both are common symptoms of gastroparesis. In the clinical trials for Ozempic, which is the same medication as Wegovy but given at a lower dose, 1 in 5 people reported nausea and 1 in 10 reported vomiting.

there would be a kind of folkloric poetic justice about this, it's very just-so story, especially regarding those who clear out stocks buying from shady "pharmacies" purely for weight loss. but in the end what we have here is mostly people who did what society and their doctors told them and are now suffering tremendously for it. people losing their jobs because they throw up too much every day to work. fucking horrific.

even better, diabetes is a risk factor for gastroparesis. diabetes. the thing other than weight loss for which these drugs are usually prescribed.

moreover. slowing the stomach is a known side effect for this medication class, but these particular, new drugs seem to have an exciting twist:

What seems to be unusual about cases like Wright’s and Knight’s, Nguyen said, is that they didn’t improve after they stopped taking the medication.

“In my experience, when you stop the GLP-1 agonist, the gastric emptying improves, and it gets better,” said Nguyen, who is also a spokesperson for the American Gastroenterological Association.

so, in at least some cases, the damage seems to be longer lasting if not permanent. who knows!!! this is medically induced dysautonomia, so of course nobody has a fucking clue.

speaking of which, here's the grimly familiar part:

Gastroparesis can have many causes, including diabetes, which is a reason many people are on these drugs in the first place. Women are known to be at higher risk for the condition, too. In more than half of cases of gastroparesis, doctors are unable to find a cause.

“They may just be really unlucky,” said Dr. Michael Camilleri, a gastroenterologist at the Mayo Clinic, said of the people who shared their cases with CNN.

On the other hand, this is how the drugs work, although not many doctors or patients understand this or the problems that may follow, he said.

same bat time, same bat channel.

there's a whole section on surgery risk, too. the reason you're supposed to fast before a surgery involving anaesthesia is to empty the stomach and minimize digestive acids, which can otherwise affect your lungs during surgery in really dangerous ways. if you're on these meds, you can follow your prep instructions perfectly and still have a full stomach when you show up. and patients often don't think to mention this med to the surgical team, because they're not aware of the connection - or even actively hide it, because being on a weight loss drug is embarrassing. anaesthesiologists are Worried.

anyway, since this sadly has to be said in the context of suffering for thinness qua beauty and patients being way too willing to accept awful side effects due to warped relationships with the medical system:

Nguyen, the Stanford doctor, said patients need to pay attention to the side effects. If you vomit once or twice, that might be normal, but persistent vomiting is not.

“They should be evaluated. Consider reducing the dose or stopping the medication,” she said.

“If your vomiting is affecting your hydration or you are having to take other medications to treat the side effects of this medication, then I think it’s time to reconsider.”

[monkeymeghan]

I posted 5,706 times in 2022

That's 2,780 more posts than 2021!

664 posts created (12%)

5,042 posts reblogged (88%)

Blogs I reblogged the most:

@bringingclawstoagunfight

@hasanyoneseenmyspoons

@spockvarietyhour

@prisma-the-spooktacular

@counting-dollars-counting-stars

I tagged 3,635 of my posts in 2022

Only 36% of my posts had no tags

#cats - 599 posts

#wordle - 301 posts

#personal - 217 posts

#comics - 214 posts

#note to self - 198 posts

#quordle - 176 posts

#tumblr - 168 posts

#quotes - 144 posts

#purr in ink - 142 posts

#jurassic park - 140 posts

Longest Tag: 102 characters

#you have to keep medications away from moisture so don’t keep them in the bathroom ‘’medicine cabinet’

My Top Posts in 2022:

#5

To those of you with cfs/me, how did you get your doctor(s) to take you seriously? I meet all of the diagnostic criteria, but over the last seven or so years since my symptoms started, everyone has chalked it up to my depression. It’s really frustrating. Since I have a new pcp, I want to make an appointment to talk to her about this since today has been terrible and my family is getting frustrated with me. I know cfs/me doesn’t have a cure, but if I have a diagnosis maybe my family could understand a bit better. (Not that I want another diagnosis, I have enough already! 😕)

23 notes - Posted October 18, 2022

#4

I have a diagnosis!! I just got off the phone with my GI doctor. I had my educated suspicions, and I was right. He went over the gastric emptying study with me, and I do have gastroparesis. I don’t have diabetes (the most common cause), so I’m one of those random unknown cause cases. Now it’s not severe, as my stomach empties like it should by the four-hour mark, but it is emptying much slower at two hours. At two hours it’s at 73% and it should be below 60%. I have to try to eat less fat and eat less soluble fiber. The doctor also wrote me a script for Reglan, which will help with both nausea and increasing gastric motility. Fingers crossed!!

23 notes - Posted June 7, 2022

#3

See the full post

28 notes - Posted November 28, 2022

#2

Chloe is holding steady. Her temp has still been good, and her weight is between 6.4 and 6.6 pounds. She’s still tiny, but she’s gained a little, and I’ll take it. She has a good appetite, and is eating great. She’s talking more and more, like she usually does. She’s even still playing a little bit. She’s even run around the house with Oscar a few times. I hope we’re out of the woods, but I don’t want to get ahead of myself.

I still have a mountain of bills from the vets, so if you can, please share this post so that my gofundme makes the rounds again. I’d really appreciate that. Thanks again for everyone who has helped me in any capacity with this, even if it’s just been sending good vibes our way.

32 notes - Posted November 16, 2022

My #1 post of 2022

See the full post

51 notes - Posted November 1, 2022

Get your Tumblr 2022 Year in Review →

[mcatmemoranda]

Reviewing questions:

Screen Asian-Americans with BMI greater than 23 for DM

I remember hearing in OnlineMedEd or something that you should replace K+ if it's below a certain level before giving insulin to pts with DKA. I told my attending this and he didn't seem to know. It was in a question I just answered:

Restoration of fluid and electrolyte deficits is the first priority when treating patients with hyperglycemic crisis. Regular insulin is usually the next intervention, given while the patient is being hydrated with the first liter of normal saline unless significant hypokalemia (serum potassium less than 3.3 mEq/L) is present. Measured serum potassium increases approximately 0.7 mEq/L for each 0.1-unit decrease in pH. Insulin therapy should be withheld until plasma potassium levels exceed 3.3 mEq/L. If insulin is given it is initially administered as an intravenous bolus of 0.1 U/kg followed by an intravenous infusion at a rate of 0.1 U/kg/hr. Alternatively, it may be given as a continuous infusion at a rate of 0.14 U/kg/hr without an initial bolus.

Restoration of fluid and electrolyte deficits is the first priority when treating patients with hyperglycemic crisis. Regular insulin is usually the next intervention, given while the patient is being hydrated with the first liter of normal saline unless significant hypokalemia (serum potassium less than 3.3 mEq/L) is present. Measured serum potassium increases approximately 0.7 mEq/L for each 0.1-unit decrease in pH. Insulin therapy should be withheld until plasma potassium levels exceed 3.3 mEq/L. If insulin is given it is initially administered as an intravenous bolus of 0.1 U/kg followed by an intravenous infusion at a rate of 0.1 U/kg/hr. Alternatively, it may be given as a continuous infusion at a rate of 0.14 U/kg/hr without an initial bolus.

The American Diabetes Association recommends that patients with type 2 diabetes engage in 150 minutes or more of moderate- to vigorous-intensity aerobic activities spread over at least 3 days each week, in addition to 2–3 sessions of resistance training each week.

Although low-fat diets have traditionally been promoted for weight loss, studies indicate that diets that provide the same caloric restriction but differ in protein, carbohydrate, or fat content are equally effective. Monitoring carbohydrate intake and its impact on blood glucose levels is key for improving postprandial glucose control.

The American Diabetes Association (ADA) has concluded that reducing overall carbohydrate intake for individuals with diabetes has the most evidence for improving glycemia and can be applied in a variety of eating patterns.

Diabetic gastroparesis has generally been attributed to disturbed gastric emptying arising from autonomic neuropathy of the gastrointestinal tract. Associated with uncontrolled and suboptimal glycemic control, it commonly presents with symptoms of nausea, vomiting, abdominal pain, early satiety, postprandial fullness, bloating, and, in severe cases, weight loss. Although upper endoscopy is required to rule out an anatomic cause, the diagnostic gold standard for gastroparesis is the measurement of gastric emptying with scintigraphy of digestible solids at 15-minute intervals for 4 hours after food intake.

Diabetic gastroparesis is generally managed with a low-fat, low-fiber eating plan with small frequent feedings and nutritional drink supplements. Withdrawing drugs with adverse effects on gastrointestinal motility, including opioids, anticholinergics, and tricyclic antidepressants, is also recommended. GLP-1 receptor agonists such as exenatide slow gastric motility and should be avoided. Pramlintide, and possibly DPP-4 inhibitors, can also impact gastric motility and should be avoided.

Incretin hormones, which include GLP-1 and glucose-independent insulinotropic polypeptide (GIP), are released from the gastrointestinal tract after a meal. These hormones are responsible for 70% of postprandial insulin secretion. GLP-1 receptor agonists appear to lower blood glucose levels by potentiating glucose-mediated insulin secretion, suppressing glucagon secretion, slowing gastric motility, and increasing satiety. Insulin glargine should not be mixed with other forms of insulin due to the low pH of its diluent. It is a long-acting, acidic insulin analog soluble only at a pH of 4.0 (as provided in the clear solution in the prescription vial). Its reduced solubility at the physiologic pH it encounters following subcutaneous injection allows for its slow absorption rate.

HbA1c normally represents a weighted average of blood glucose levels during the preceding 120 days, which is the lifespan of a normal red blood cell. Any condition that prolongs the life of the erythrocyte or that is associated with reduced red cell turnover exposes the red cell to glucose for a longer period of time, resulting in higher HbA1c levels. Conditions associated with decreased red blood cell turnover include iron deficiency anemia, vitamin B12 deficiency, folate deficiency, and asplenia. Conversely, any condition that shortens the lifespan of the erythrocyte or that is associated with increased red cell turnover would tend to produce lower HbA1c levels. Examples would include hemolytic anemia, splenomegaly, and acute and chronic blood loss. Vitamin E ingestion has also been associated with lower HbA1c levels, presumably by interfering with glycation.

The GLP-1 receptor agonists such as exenatide and liraglutide are most likely to result in weight reduction.

The estimated prevalence of diabetes mellitus among adults was 7.4% in 1995 and is projected to rise to 9.0% by 2025. Screening every 3 years is recommended in asymptomatic adults beginning at age 45 in the absence of risk factors. Screening should be considered at an earlier age in patients who have a BMI ≥25 kg/m2 and one or more of the following additional risk factors:

• physical inactivity • a first degree relative with diabetes • a history of cardiovascular disease • a Native American, Black, Hispanic, Asian, or South Pacific Islander race/ethnicity • a blood pressure ≥140/90 mm Hg or receiving drug treatment for hypertension • an HDL-cholesterol level less than 35 mg/dL • a serum triglyceride level >250 mg/dL • a medical condition associated with insulin resistance, including acanthosis nigricans or severe obesity • a history of polycystic ovary syndrome, gestational diabetes, or delivering an infant weighing more than 4 kg (9 lb)

Insulin resistance is also found in more than half of patients without diabetes who experience an ischemic stroke or TIA. In the IRIS trial, the use of pioglitazone was associated with a 24% reduction in stroke and myocardial infarction and a 52% reduction in the risk of developing type 2 diabetes.

For patients with diabetes who are at high cardiovascular risk and whose cholesterol levels are controlled with statin therapy but who have elevated serum triglycerides (135–499 mg/dL), the American Diabetes Association (ADA) recommends the addition of icosapent ethyl (Vascepa) to reduce cardiovascular risk. Icosapent ethyl is highly purified eicosapentaenoic acid (EPA) ethyl ester fish oil. Use of this agent is supported by the REDUCE-IT trial. Use of icosapent ethyl resulted in a 25% reduction in the relative risk of the primary combined endpoint of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, or unstable angina during a mean follow-up period of 4.9 years. This type of benefit has not been demonstrated in trials of other omega-3 fatty acid products and the lack of benefit from these other products may be related either to dosage differences or to their lower ratio of EPA to docosahexaenoic acid (DHA). The ADA has therefore recommended that the benefits of REDUCE-IT not be extrapolated to other omega-3 fatty acid products.

Niacin, which not only reduces serum triglycerides and LDL-cholesterol but raises HDL-cholesterol as well, has also not been shown to reduce cardiovascular risk when used in combination with a statin. Bile acid–binding resins such as cholestyramine and colestipol raise serum triglycerides and are contraindicated in hypertriglyceridemia.

In patients with dyslipidemia, lowering triglycerides with fenofibrate may slow the progression of diabetic retinopathy, particularly in those with very mild nonproliferative diabetic retinopathy at baseline.

For patients of all ages with diabetes mellitus and atherosclerotic cardiovascular disease, the American Diabetes Association (ADA) guidelines recommend that high-intensity statin therapy be added to lifestyle therapy. However, a high risk of myopathy and rhabdomyolysis is associated with high-dose simvastatin, and in 2012 the FDA issued a safety alert advising that the 80-mg dose of simvastatin be used only in patients who have been taking this dosage for 12 months or more without evidence of muscle toxicity. In this patient, simvastatin should be discontinued and another statin such as atorvastatin or rosuvastatin should be prescribed.

A supervised exercise program has been shown to improve functional status, walking distance, and quality of life in patients with peripheral artery disease. Although its use has not been associated with reduced cardiovascular risk or improved quality of life, cilostazol has been shown to improve walking distance. The use of low-dose aspirin (75–162 mg daily) is recommended by the ADA for diabetic patients with existing atherosclerotic vascular disease.

Claudication does not progress to critical limb ischemia in most patients with peripheral artery disease, with reported rates below 10%–15% over a period of 5 years or more. Given the risk of adverse procedural events, such as bleeding, renal failure from contrast-induced nephropathy, and the possibility of adverse limb outcomes, and the lack of proven benefit, the American Heart Association strongly recommends against surgical or endovascular intervention to prevent disease progression.

the choice of medication added to metformin should be based on the clinical characteristics and preferences of the patient. Considerations include cardiovascular risk, the presence of atherosclerotic cardiovascular disease, comorbidities, cost, safety, tolerability, and risk of adverse side effects. Although there is some evidence that metformin may reduce the risk of cardiovascular events and death, the evidence is most robust for SGLT2 inhibitors [-flozins]and GLP-1 receptor agonists [-glutides such as liraglutide, dulaglutide]. Large randomized, controlled trials have demonstrated significant reductions in cardiovascular events in patients with type 2 diabetes treated with an SGLT2 inhibitor such as empagliflozin, canagliflozin, or dapagliflozin, or a GLP-1 receptor agonist such as liraglutide, semaglutide, or dulaglutide.

For patients with type 2 diabetes, the ADA recommends that an SGLT2 inhibitor or a GLP-1 receptor agonist should be strongly considered, independent of baseline hemoglobin A1c or the individualized hemoglobin A1c target, for those with established atherosclerotic cardiovascular disease or indicators of high atherosclerotic cardiovascular risk, established kidney disease, or heart failure.

Indicators of high cardiovascular risk include a patient >55 years of age with left ventricular hypertrophy, or with coronary, carotid, or lower-extremity artery stenosis >50%.

Studies support a link between statin use and the development of diabetes mellitus. Intensive-dose statin therapy was associated with a higher risk of new-onset diabetes compared with moderate-dose statin therapy. In 2012, the FDA modified the package labeling of statins to include the risk of increased blood glucose levels and the development of type 2 diabetes. The benefit of statin therapy, however, outweighs the risk. It has been estimated that although use of statin therapy may cause one additional case of diabetes for every 498 patients treated for 1 year, its use also results in one less patient experiencing a cardiovascular event for every 155 patients treated for 1 year.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver disorders and is strongly associated with obesity, insulin resistance, and type 2 diabetes. 20% develop nonalcoholic steatohepatitis (NASH), which by definition includes fibrosis, and 20% of patients with NASH will develop cirrhosis. Patients with steatosis are at higher risk for NASH if they are obese or have glucose intolerance, hypertension, hypertriglyceridemia, or metabolic syndrome.

NAFLD is often suspected on the basis of mildly elevated plasma aminotransferases or vague abdominal symptoms such as right upper quadrant pain. The degree of aminotransferase elevation does not predict the degree of hepatic inflammation or fibrosis, and a normal alanine aminotransferase level does not exclude a clinically important histologic injury or the presence of NASH. The diagnosis of NAFLD is typically based on hepatic steatosis found on liver ultrasonography. Scoring methods such as the FIB-4 can be used to determine if there is a risk of NASH and whether further testing such as a liver biopsy is indicated.

Lifestyle modification, particularly weight loss and exercise, represents the cornerstone of therapy. Weight loss, whether achieved by lifestyle changes or bariatric surgery, has been shown to have the greatest benefit on histologic improvement, with a recommended target weight loss of 7%–10%. Although there is some evidence to suggest that vitamin E and pioglitazone improve liver histology in NASH, there are no FDA-approved agents for treatment of NASH. It is generally recommended that patients with NAFLD avoid alcohol use. The presence of elevated hepatic transaminases in NAFLD does not contraindicate statin use, and guideline-directed medical therapy, which includes statin use, is recommended in patients with NAFLD because of their increased cardiovascular risk.

Resistant hypertension is present when the blood pressure of a hypertensive patient remains elevated above goal despite the concurrent use of three antihypertensive agents of different classes at adequate doses, including a diuretic. For patients with diabetes mellitus diagnosed with resistant hypertension, the American Diabetes Association guidelines recommend considering a mineralocorticoid receptor antagonist such as spironolactone.

Diabetic nephropathy develops in 20%–40% of patients with diabetes mellitus and is the leading cause of end-stage renal disease. Persistent albuminuria in the range of 30–200 mg/24 hr (microalbuminuria) is the earliest sign of nephropathy in patients with type 1 diabetes and is a marker for nephropathy in type 2 diabetes. Patients with microalbuminuria who progress to macroalbuminuria (>300 mg/24 hr) are likely to progress to end-stage renal disease over a period of years.

A random spot urine specimen for measurement of the albumin/creatinine ratio is the preferred method. A minimum of two of three tests showing a urine albumin level >30 µg/mg creatinine over a 6-month period confirms the diagnosis of microalbuminuria.

Intensive diabetic management and the use of ACE inhibitors and angiotensin receptor blockers (ARBs) have been shown to delay the progression from microalbuminuria to macroalbuminuria in patients with type 1 or type 2 diabetes.

current American Diabetes Association (ADA) guidelines recommend the use of either an ACE inhibitor or an ARB for those with a modestly elevated urinary albumin/creatinine ratio (30–299 mg/g creatinine) and strongly recommend them for those with a urinary albumin/creatinine ratio ≥300 mg/g creatinine.

ADA guidelines recommend against the use of these drugs for patients with normal blood pressure and no albuminuria.

The American Diabetes Association (ADA) recommends that patients of all ages with diabetes mellitus and atherosclerotic cardiovascular disease (ASCVD) should have high-intensity statin therapy added to lifestyle therapy

Aspirin at a dosage of 75–162 mg daily is recommended by the ADA as a secondary preventive strategy in patients with diabetes and a history of cardiovascular disease. The ADA also states that low-dose aspirin therapy could be considered as a primary prevention strategy for those with type 1 or type 2 diabetes who are at increased cardiovascular risk and not at increased risk of bleeding.

The LEADER trial (Liraglutide Effect and Action in Diabetes: Evaluation of cardiovascular outcome Results) was a double-blind trial that compared the use of liraglutide, a GLP-1 analogue, to placebo in 9340 patients with type 2 diabetes at high cardiovascular risk. After a mean follow-up of 3.8 years, liraglutide was found to significantly reduce the rate of death from cardiovascular causes, as well as the first occurrence of nonfatal myocardial infarction and nonfatal stroke

thiazolidinediones are associated with fluid retention, which can lead to weight gain, edema, and heart failure. Their use is contraindicated in patients with New York Heart Association class III or IV heart failure.

a weight reduction as small as 5%–10% was found to lower the risk of developing diabetes.

The American Diabetes Association recommends that patients with prediabetes achieve and maintain a minimum weight loss of 7%–10% and exercise a minimum of 150 minutes per week.

Metabolic syndrome is a constellation of cardiovascular risk factors related to hypertension, abdominal obesity, dyslipidemia, and insulin resistance. Ddiagnostic criteria for metabolic syndrome include the presence of three or more of the following:

• obesity, with a waist circumference exceeding 102 cm (40 inches) in men or 88 cm (35 inches) in women • blood pressure ≥130 mm Hg systolic and/or 85 mm Hg diastolic • a fasting glucose level ≥110 mg/dL • a serum triglyceride level ≥150 mg/dL • an HDL-cholesterol level less than 40 mg/dL in men or less than 50 mg/dL in women

[diabetes-health-corner]

Type 2 Diabetic Gastroparesis: Causes, Symptoms and Treatment

In this blog, we'll break down everything you need to know about Type 2 Diabetic Gastroparesis – from causes and risk factors to diagnosis and treatment options.

Read the full blog here: https://www.freedomfromdiabetes.org/blog/post/type-2-diabetic-gastroparesis-causes-symptoms/3496

[drnishargpatel]

Understanding the Link Between Diabetes and Digestive Problems

Diabetes is a chronic condition that affects millions of people worldwide. While most people are familiar with the impact diabetes has on blood sugar levels and overall health, many are unaware of the connection between diabetes and digestive problems. Navigating Digestive Health in Diabetes: Key Considerations is essential because individuals with diabetes often experience digestive issues, which can significantly affect their quality of life.

Gastroenterologist in Surat can provide insight into how diabetes affects digestion and offer specialized care. Understanding this link is crucial for better managing both conditions. In this article, we will explore how diabetes affects digestion, common digestive problems associated with the condition, and practical steps you can take to manage these symptoms.

How Diabetes Affects Digestion

Nerve damage (diabetic neuropathy): Long-term high blood sugar levels can cause nerve damage, particularly affecting the vagus nerve, which controls digestion.

Slow digestion: Damage to the vagus nerve leads to gastroparesis, where the stomach takes too long to empty its contents, causing digestive problems.

Irregular movement: Nerve damage results in slow or erratic movement of food through the digestive tract, affecting overall digestive health.

Common Digestive Problems in Diabetic Patients

Gastroparesis:

Condition where stomach emptying is delayed.

Symptoms include nausea, vomiting, bloating, and feeling full quickly.

Leads to erratic blood sugar levels, complicating diabetes management.

Constipation:

Common due to nerve damage affecting bowel movement.

Causes infrequent or difficult bowel movements.

Leads to bloating, abdominal discomfort, and potential for more serious conditions.

Diarrhea:

Caused by autonomic neuropathy, where nerve damage accelerates intestinal contractions.

Leads to frequent, loose stools, causing dehydration and blood sugar fluctuations.

Heartburn and Acid Reflux:

Delayed stomach emptying causes acid to rise into the esophagus, leading to heartburn.

Results in discomfort and requires dietary adjustments or medications.

Celiac Disease:

More common in type 1 diabetic patients.

Immune response to gluten damages the small intestine.

Leads to nutrient malabsorption, further complicating diabetes management.

Managing Digestive Problems with Diabetes

Control Blood Sugar Levels:

Keep blood sugar levels stable to minimize nerve damage and prevent digestive issues.

Regular blood glucose monitoring, medication adherence, and healthy eating are key.

Dietary Adjustments:

Smaller, frequent meals help with gastroparesis and keep blood sugar stable.

High-fiber foods like fruits, vegetables, and whole grains help relieve constipation (caution for gastroparesis patients).

Hydration: Drink plenty of water to ease digestion and prevent constipation and dehydration.

Exercise Regularly:

Stimulates digestion and regulates blood sugar levels.

Walking after meals can improve digestion and reduce constipation.

Medication for Digestive Problems:

Prokinetics: Improve food movement through the digestive tract, especially in gastroparesis cases.

Laxatives: Help relieve constipation when lifestyle changes aren’t enough.

Antidiarrheal Medications: Used to slow bowel movements for chronic diarrhea.

Antacids or Proton Pump Inhibitors: Reduce acid and relieve heartburn or reflux symptoms.

When to See a Doctor:

Seek medical advice for persistent or severe symptoms like nausea, vomiting, weight loss, or chronic digestive issues.

Early medical intervention helps prevent complications and improve quality of life.

Conclusion

The link between diabetes and digestive problems is undeniable, with high blood sugar levels often causing nerve damage that disrupts the digestive system. However, with careful management of blood sugar levels, dietary changes, regular exercise, and appropriate medical intervention, many digestive issues can be alleviated or even prevented. By understanding the connection between diabetes and digestion, individuals can take proactive steps to protect their digestive health and enjoy a better quality of life.

Always consult with a healthcare professional to find the best approach for managing your symptoms and maintaining both your digestive and overall health.

[cannabiscomrade]

I have found one study that associates non-diabetic insulin resistance in people with PCOS with gastroparesis and I really just want to stress the fact that we know so little about PCOS truly outside the fertility impacts

I am still investigating my cause of GP but realizing that it could be the result of my intersex condition is staggering. I have so many symptoms/conditions like reactive hypoglycemia and gastroparesis that mirror complications of diabetes while my A1C and other levels are in range to indicate it’s not diabetes but my PCOS

[thewolfwaitsbelow]

When I had my big gastroparesis flare up and got diagnosed I always paused when the symptom questionnaire asked if I was experiencing “unexplained weight loss” because like. I knew why I was losing weight it’s bc I couldn’t eat hardly anything.

Like with undiagnosed type 1 diabetes you get unexplained weight loss where you eat like normally and still lose weight because your body can’t process most of it. That was my bench mark for unexplained weight loss.

My mom was like “you lost 20lbs in less than a month check yes” but in my mind my weight loss was very well explained. I stopped eating. Clear cause and effect. Why I couldn’t eat was the real question

[susantaylor01]

How does diabetes affect the body?

Simple Technique To Help Manage Blood Sugar

Introduction

Diabetes is a chronic health condition that impairs the body’s ability to process glucose, the primary source of energy for cells. This inability stems from issues related to insulin, a hormone produced by the pancreas, which is essential for regulating blood sugar levels. There are two main types of diabetes: Type 1, where the body fails to produce insulin, and Type 2, where the body either does not produce enough insulin or cannot effectively use the insulin it produces. Both types lead to elevated blood glucose levels, a condition known as hyperglycemia, which can have widespread effects on the body.

1 . Blood Vessels and Cardiovascular System

One of the most significant impacts of diabetes is on the cardiovascular system. Chronic high blood sugar levels can damage the blood vessels and the nerves that control the heart and blood vessels. This increases the risk of developing heart disease, stroke, and other cardiovascular complications. Diabetic individuals are more likely to develop atherosclerosis, a condition characterized by the hardening and narrowing of the arteries due to the buildup of fatty deposits. This can lead to reduced blood flow, increasing the risk of heart attacks and strokes.

In addition, diabetes can lead to high blood pressure, which further stresses the heart and blood vessels. Hypertension, when combined with diabetes, greatly elevates the risk of cardiovascular events. Over time, the cumulative damage to the cardiovascular system can lead to heart failure and other severe complications.

2. Kidneys and Renal System

Diabetes is one of the leading causes of kidney damage, a condition known as diabetic nephropathy. The kidneys' primary function is to filter waste products from the blood and excrete them in the urine. However, high blood sugar levels can damage the blood vessels in the kidneys, impairing their ability to filter waste effectively. Over time, this damage can lead to kidney failure, requiring dialysis or a kidney transplant.

Diabetic nephropathy usually develops slowly over several years and may not cause symptoms in its early stages. However, as the damage progresses, it can lead to proteinuria (the presence of excess protein in the urine), swelling in the feet and ankles, and eventually, complete kidney failure. Regular monitoring of kidney function is crucial for individuals with diabetes to detect and manage this condition early.

3. Nervous System and Neuropathy

Diabetes can cause damage to the nervous system, a condition known as diabetic neuropathy. High blood glucose levels can injure the walls of tiny blood vessels that nourish the nerves, particularly in the legs. This can lead to a variety of symptoms, including pain, tingling, numbness, and weakness, usually starting in the extremities and spreading upwards. In severe cases, this can result in loss of sensation, increasing the risk of injuries that go unnoticed and develop into serious infections.

There are different types of diabetic neuropathy, including peripheral neuropathy, autonomic neuropathy, proximal neuropathy, and focal neuropathy. Each type affects different parts of the body, leading to a wide range of symptoms. For instance, autonomic neuropathy can affect the nerves that control the bladder, leading to urinary problems, or the nerves that control digestion, leading to issues like gastroparesis.

4. Eyes and Vision

Diabetes can also have a profound effect on vision. High blood sugar levels can damage the blood vessels in the retina, the light-sensitive tissue at the back of the eye, leading to a condition known as diabetic retinopathy. This condition is one of the leading causes of blindness in adults. In its early stages, diabetic retinopathy may not cause any symptoms, but as it progresses, it can lead to vision loss.

Diabetes also increases the risk of other eye conditions, including cataracts, where the lens of the eye becomes cloudy, and glaucoma, a condition characterized by increased pressure in the eye that can damage the optic nerve. Regular eye exams are essential for people with diabetes to detect these conditions early and manage them before they lead to significant vision loss.

5. Skin and Wound Healing

The skin is another organ that can be significantly affected by diabetes. High blood sugar levels can impair circulation, which reduces the skin’s ability to heal properly and increases the risk of infections. This is particularly concerning for individuals with diabetic neuropathy, as they may not notice minor injuries that can quickly become serious infections. Common skin conditions associated with diabetes include bacterial infections, fungal infections, and diabetic dermopathy, which causes brown, scaly patches on the skin.

Diabetes can also slow the healing process, making it harder for the body to recover from wounds. This is especially dangerous in the case of foot ulcers, which can develop in people with diabetic neuropathy. If left untreated, these ulcers can lead to severe infections that may require amputation.

6. Digestive System

Diabetes can also affect the digestive system. Autonomic neuropathy can damage the nerves that control the stomach, leading to a condition known as gastroparesis. This condition slows down or stops the movement of food from the stomach to the small intestine, causing symptoms such as nausea, vomiting, bloating, and abdominal pain. Gastroparesis can make it difficult to control blood sugar levels, leading to further complications.

In addition, people with diabetes are at an increased risk of developing other digestive conditions, such as acid reflux, irritable bowel syndrome, and fatty liver disease. Managing blood sugar levels through diet, medication, and lifestyle changes can help mitigate these effects on the digestive system.

Conclusion

Diabetes is a complex and chronic condition that affects nearly every part of the body. Its complications range from cardiovascular issues and kidney damage to nerve damage and vision problems. Understanding how diabetes affects different organs and systems is crucial for managing the disease and preventing its complications. Regular monitoring, a healthy lifestyle, and adherence to treatment plans are essential for minimizing the impact of diabetes on the body and maintaining overall health.