H63D Genes, Hemochromarosis, Multiple Sclerosis, iron

 Wild. --- unmutated h63D gene (gray) and mutated H63D gene (red)

Back to this pesky H63D gene needing to write again on. 

This does concern the Primary Progressive Multiple Sclerosis disease I was given in 2012, and the multitude of diagnosis that came afterwards, all inter related.  I hope some scientist can figure this out.

Pro570Ser - risk allele: T (Pro589Ser) This is called TF C2. It creates an increased likelihood of iron loading when combined with any c282y and h63d because it forces a reduced TIBC resulting in higher levels of free iron and free radicals. This also Increases susceptibility to Alzheimer's disease but only when combined with c282y.

But I have two copies of H63D, that one less than 3% get iron overloaded.

This gene has been With me my entire life. It is hereditary.

My Iron Results DNA

Hemochromatosis is one of the diagnosis in 2018. Thick blood, that the endocrinologist sent me to the Cancer Center. It took them a few DNA searches to find, but two pair. Less than 3% have Hemochromatosis caused by this gene.  My Iron, Hemoglobin, Hematocrit, Transferrin were high, along with Hypertrycglimeria stage I was in.

17 phlebotomy or vein punctures for my Europe readers were done last quarter of 2018.

Two years later, no iron has returned (or a little, since they allowed me to use cast iron skillet again, and spinach) but iron still low, barely on the chart.

My blood was thicker than pancake batter.

Does this still make me anemic two years later? Depends on which Doctor you talk with

Is this being anemic for two years? I kept doing my blood labs every two months. with iron not moving. The hemoglobin is on high side now.  So does this make me iron deficient?

Lots of questions, so asked my medical team.

Ferritin 13, iron 49, Transferrin 305H, Total iron binding 424H, Iron sat11.6% low. This is two years after phlebotomy Erythropietin was 25H. Creatine still high, along with Tryglicerdimia

As anemic, has its own set of problems, and other diagnostic items of what it can damage, and so does low iron, and MS.

I belong to a Hemochromatosis group. had family checked, as hereditary.   Found two others given diagnostic from this pesky gene. I asked to become a member of anemia group, and iron group to find out more of what came first?

What if I had anemia my whole life, but it was drowned out by Hemochromatosis, and MS? I found a site,  https://www.anemiaid.com/

This will check your DNA for free.  I sent request to my cancer Dr.

I also found interesting info from these sites I emailed my Dr team.

https://www.rethinkanemiaofckd.com/insufficient-hif-activation.html

https://www.niddk.nih.gov/health-information/blood-diseases/anemia-inflammation-chronic-disease#chronic

My GI symptoms went south when I had my last phlebotomy. He did not see coordination of iron playing a role. He is a great GI Dr.  Linzess along with laculose was given. He informed me from my last upper and lower GI, that I did not have ulcerative colitis, but  IBS-C. He did more test to verify this. A breathing test to check for hydrogen. Used  l lactulose, so had to be off this for a week. Constipation.  A emptying test.

I have also had a swallowing test, that showed problems. Eating radioactive food, never sound appealing.

I am also on metoclopramide, as my MS is not giving my bowel muscles the proper signal to muscles to move food along. This was also tested, by going off this medicine for months, and being put back on. I call this a Black Box medicine, as may interfere with my other meds. My drug company always has to check with GP, Neurologist, and GI Dr to get ok.

But GI problems go with MS, hand in hand. However, if you do not have iron, another story.

Iron is a absorbed in the lower intestine.

I have problems absorbing items there, as a test with vitamin D was done, with the assistance of my endocrinologist.  I was able to take 50,000 iu/day less tablets, by just changing time of day taken. A oil pill, like Vascepa, but interference with some genes and possibility meds.  

Not that Iron is the solution, but why am I not absorbing from foods, cast iron skillets? 

If regular Hemochromatosis, I would be making new red blood cells every four months. The bone marrow, would tell this. Also I would need to give blood every three months for Hemochromatosis levels.

So not to go into any new diagnosis given, I asked my team at UC Davis to check on more items. This may add a new team member, but that's for another blog.

Would love feedback from anyone.

Stay health and safe.  Be sure to like my blog and YouTube channel.

JoeY

MS, H63D Hemochromatosis Are Associated with Primary Hypertriglyceridemia

Hypertriglyceridemia the thought of the day.

 The association with Multiple Sclerosis, the H63D gene mutations, and what it is.

high level of a certain type of fat (triglycerides) in the blood.

• Treatable by a medical professional
• Requires a medical diagnosis
• Lab tests or imaging always required
• Chronic: can last for years or be lifelong

Elevated triglycerides may contribute to many items,  much to many to get people excited without blood tests, and talk about in this blog.  My next blood tests are at the end of the year, followed up in January 2021 by a endocrinologist, my cancer Doctor, GP, and heart Dr., along with others.

Most people with elevated triglycerides experience no symptoms.

https://academic.oup.com/jcem/article/94/11/4391/2596710

Mutations in HFE Causing Hemochromatosis Are Associated with Primary Hypertriglyceridemia

My Journey through Hypertriglyceridemia goes on for years now. When the levels of Iron were extremely high the summer of 2018, my tryglicerides were also in the Hypertriglyceridemia stage. The inter relationship of this and high iron , Hemochromatosis, caused by the the gene mutations of both H63D genes, is quite rare, and listed in rare diseases.

When my first thru seventeen phlebotomy or vein puncture were done to remove blood from me weekly, that started October 2018, my mind set was on the rare H63d genes involved, and the iron.

My Tryglicerides dropped in half after the phlebotomy, or vein punctures were done early 2019.  But that still left me with Hypertriglyceridemia going on.  My Heart Dr tried a drug known as Fenofibrate with me. Since the Heart is a muscle, and can be affected by multiple Sclerosis, he has been thru me on this entire journey as part of my "MD Team"

For those now curious, my heart Has always been fine. EKG done many times by many Drs. A Echo of the heart is done yearly, always looking good.  My Cholesterol levels looks great. My Heart Races like I am in a Marathon, even if sitting still. This is caused by MS.

I use a app, my heart or blood pressure designed by 

Http:www/Klimaszewski.mobi

Great app. I use a cuff on arm to put data into this App, or data from different Drs gives me many results. Shows when I was put on a heart pill, to lower readings, and data back many years. Of highs and lows.  This shows a GP not giving me a EKG, and his report even shows how high. It was my first and last appointment with him.

The Fenofibrate I became extremely allergic to. I was one of less than 3% that had a negative reaction, being caught by my Endocrinologist. Three days off, dropped my readings. Vascepa was the next Medicine to try by my Heart Dr.  This is like taking 34 omega 3 fish oil pills, but put into each 1 Gram Pill. 4 Grams daily. No fishy taste or burps.

But is supposed to help tryglicerides.

My Cholesterol is normal.

Berberine hcl, and Taurine, red yeast rice, CoQ10, along with other natural substances are supposed to help. I would check with your Dr before trying anything I have listed, as I am not a Dr.

H63D & S65C ~ The Forgotten HFE (Haemochromatosis) Mutations

Private group on Facebook is a great source of information.

1 in 100

Medications used in the management of hypertriglyceridemia include the following:

Fibric acid derivatives (eg, gemfibrozil, fenofibrate)

Niacin (slow-release, immediate-release, extended-release formulations)

Omega-3 fatty acids (eg, icosapent, omega-3-acid ethyl esters)

HMG-CoA reductase inhibitors (eg, atorvastatin, fluvastatin, pitavastatin, pravastatin, lovastatin, simvastatin, rosuvastatin)

The diagnosis is made on blood tests, often performed as part of screening. Once diagnosed, other blood tests are usually required to determine whether the raised triglyceride level is caused by other underlying disorders ("secondary hypertriglyceridemia") or whether no such underlying cause exists ("primary hypertriglyceridaemia"). There is a hereditary predisposition to both primary and secondary hypertriglyceridemia.[1]

Sending me notes or any info on tryglicerides will always be helpful. This is a gene handed down generations ago.

H63d/H63d means I will always be watched for iron. The tryglicerides connection is something newly found, and other members have chimed in stating the same.

Thanks for reading 

Joey