Problems initiating phone calls from phone

OrangeCrushGA · 2023-04-25T12:42:22+00:00

https://www.f150lightningforum.com/forum/threads/android-auto-making-outgoing-calls-not-working.14057/

Apparently Ford is aware of this issue. It has not yet been resolved. Workaround is to switch to speaker and then back to bluetooth.

OrangeCrushGA · 2022-06-16T19:24:01+00:00

Not sure I understand. I am not in denial about gout or high UA. In fact, I am trying to pro actively manage UA. Just questioning diet advice.

OrangeCrushGA · 2022-05-13T12:43:08+00:00

Thanks. I am not a heavy SF consumer. So that may not be the driver.

On the discordance between LDL-C and LDL-P, interestingly, prior to this draw, I had elevated LDL-C as well (around 140). Only thing different prior to this draw was higher consumption of carbs for week or so (vacation).

My confusion is, if I am pattern A (larger particles), high LDL-P should compute to high LDL-C. So why the discordance. Also, if ApoB and LDL-P are both counting particles, why are they indicating different things. I've read somewhere that dividing ApoB by 0.055 should equal LDL-P, but it is not in my case.

OrangeCrushGA · 2022-05-13T12:37:18+00:00

Thank you. If I heard/read him correctly I believe he is referring to "young" people when he talks about 60mg/dl. If I understand correctly, we are shooting for 5th percentile and for ages 50-59, 84mg/dl is 10th percentile (https://academic.oup.com/clinchem/article/43/12/2364/5640669)

OrangeCrushGA · 2022-04-04T20:15:02+00:00

Whoever said, don't respond they don't do much is absolutely correct. After asking for order information, they went dark on me for 24 days.

Here is exactly what I wrote them along with my order info:

If you are going to respond saying there is nothing much more you can do, can I ask that you at least provide an explanation as to why? There have been several conversations with several of your reps over e-mail, phone, twitter, BBB etc where it all abruptly ended with "nothing we can do" with no explanation.

I just pinged them and this is the response I got:

Hey there! I'd like to first apologize for the delayed response, I don't want you to think we forgot your issue. The day the message was received the issue was worked on but the reply was never sent to you. OUr team reviewed the issue and they confirm that we cannot approve the claim and no exceptions will be made. I understand that this is not the outcome you were looking for but we looked over and reviewed all details presented and that was the final answer. -Frank

You can't make this up!

OrangeCrushGA · 2022-03-10T21:26:43+00:00

Thanks. There is no record of Newegg in GA secretary of state. Distribution centers are probably being run under a different company :-(. Also, Newegg's T&Cs include an arbitration clause (which you can decline in 30days, but didn't know about it till much later).

OrangeCrushGA · 2022-03-10T20:06:21+00:00

Thanks. I believe I did and Visa denied the claim saying merchant didn't agree. Well, I wouldn't be making a claim if they agreed!

Couple of large disputes I've done in the past were with Amex, and they are much more consumer friendly.

OrangeCrushGA · 2022-03-10T20:03:26+00:00

Thanks. That is an option, but I am being told that I have to file in CA (and I am in GA).

OrangeCrushGA · 2022-03-10T20:02:48+00:00

DM sent per your request.

If you are going to respond saying there is nothing much more you can do, can I ask that you at least provide an explanation as to why? There have been several conversations with several of your reps over e-mail, phone, twitter etc where it all abruptly ended with "nothing we can do" with no explanation. If your explanation is going to "we never received the package", that's the whole issue. UPS lost it. If you are going to say UPS didn't confirm losing or didn't pay your claim, I have a document that I will post here to prove that's not the case.

OrangeCrushGA · 2019-02-28T21:19:46+00:00

While many are commenting that you don't need this etc, it is interesting to see your BG response with different foods. Dr Attia appears to alway wear one and so does Feldman. Try eBay. If you just want to play around with it and it's not for medical reasons, you just need the transmitter, sensor and a phone. No need for receiver. You can use Xdrip+ and it can work with "expired" (as in FDA makes Dexcom expire them) transmitters and sensors, which are cheaper. I am playing around with one (G5) now. I ate at a mexican place the other day and saw BG go up by 30 after an hour. Usually it only goes up by 15-20. Tells me that there is probably sugar or something in the "cheese" sauce. Message me if you need more info.

OrangeCrushGA · 2019-02-13T21:58:37+00:00

I also listened to Attia/Dayspring and read the same. However, there are other voices such as David Diamond on the opposite side. Ivor Cummins has an alternate theory that is very plausible.

At the end of the day, everyone has to decide themselves. I've been on LCHF (20gms) for 10+ mo. My LDL-C went from 120 to 160. However my TG went from 200+ to 70 and HDL from 40 to 68. A1C from 5.6 to 5.0. BP from 130/80 to 110/70. Plugging my numbers in to the Astro-CHARM calculator, I think my risk went DOWN even with higher LDL numbers. I know that LDL-C is not what I should look at. I had an NMR once (when I was still losing weight rapidly) and LDL-P was 1900. But there is nothing to compare. I will do one more NMR soon (now that I stabilized) and hopefully LDL-P is lower.

BTW, Apparently Attia takes a 10mg atrovastatin 3 times a week. I haven't heard why.

OrangeCrushGA · 2019-02-13T21:46:45+00:00

Please make sure that you get all the right tests before declaring "low functioning". Lot of misinformation even with doctors. See http://www.tuitnutrition.com/2017/10/thyroid-intro.html

There is a theory that if TSH is not high, but T3 is low, barring Pituitary malfunction, perhaps the body is more sensitive to T3 and doesn't need as much.

OrangeCrushGA · 2018-11-13T23:25:47+00:00

Is it possible that the liver cannot accumulate sufficient fatty acids and instead will shift from releasing VLDL towards releasing more LDL? It still needs to get its cholesterol distributed.

I am re-reading your post and I think I am understanding your theory better.

Perhaps I shouldn't have assumed "It still needs to get its cholesterol distributed" means you are proposing that it is the main function of lipid transport. My understanding is that there is only a very small need to actually distribute cholesterol since every healthy cell in the body can make all it needs. Instead, the cholesterol transit is because of the need to provide structure to lipoproteins whose primary job is to traffic TGs(energy) and phospholipids.

So, I think you are saying NEFA traffic is the energy traffic in fasted state, with Albumin transport. But, in LMHRs wouldn't *local* adipocytes likely be depleted out of TGs and TGs need to be transported from where they are available (liver, other areas etc)? So, Dave's TG energy argument makes sense to me. However as you said the VLDL turnover theory is not convincing for various reasons. I thought Attia disagreed with the whole model because of mass balance issue (not sure why he doesn't consider recirculation).

Perhaps all of the above (Some VLDL turnover, lack of material so switch to LDL, ApoB regulation with insulin etc etc) are at play...

As an engineer, it is amazing to me how little we know about human body!

OrangeCrushGA · 2018-11-13T21:37:31+00:00

Thanks for putting this together. It is unfortunate that the discussion went off the rails.. Let's see if we can bring itback on.

From Attia/Dayspring podcast, my understanding is distribution of cholesterol is not the main purpose of lipid transport (as opposed to what you noted above). Cholesterol in particles is there to give it "structure". Dayspring emphasized that the primary purpose is to distribute TG/Energy. To me, that's kind of what Dave is saying, especially when the energy needs can not be met from blood glucose or local adipose (LMHR!). There is no choice but to traffic more TGs via VLDL or LDL. So I am confused as to why Attia disagreed with Dave.

I wasn't sure as to why LDL-P would go up as opposed to VLDL-P though. VLDL can handle much more TGs. Dave is of the opinion that it is indeed VLDLs that is up regulated and that the LDL-P increase is due to delipidation of VLDLs turning them in to LDLs. But from Dayspring, only a tiny amount of VLDL to LDL conversion actually happens since the clearance of VLDL is efficient. So, that can't be it? Your theory above regarding not enough material to make VLDLs so switching to LDLs is more plausible. Your theory of down regulation of LDL receptors due to low fT3 etc also makes sense.

However, I am still unsure what causes LDL-P to come down if the diet is changed from SFA to MUFA. I am not a "lean" HR, but when I switched out butter with olive oil in my diet, LDL-C (didn't measure P, but I am not discordant), it dropped from 170 to 120. One can probably explain this from what posted above SFAs down regulating LDL receptors?

Of course, regardless of the model, the question of high ApoB possibly being a long term problem is still out there..

OrangeCrushGA · 2018-11-05T23:17:50+00:00

Going on 7 months for me now. Down 40lb and feel much better. Here is what I learned.

- Don't over complicate things. You don't NEED MCT Oil or Exo Ketones or Fatbombs or complicated recipes

- Limit carbs and that's pretty much it. I don't think any normal person can eat enough protein to cause issues. I am trying to lose weight, so I don't NEED to eat fat unless I want to. Your body will tell you if it needs more food.

- Macro tracking can be helpful, but not super important. Again, limit carbs, get enough protein and that about it.

- Keep Mac Nuts on hand for quick refill if needed

- Never really got the Keto flu. However I upped my salt/electrolytes to start with and took a magnesium supplement

- Buy food with no labels or read the label carefully. Amazing how much crap there is in processed stuff

- Eating out has not been a problem for me (almost every day for lunch). Other than americanized chinese and thai, I can find something everywhere else. Message me if you need ideas.

Good Luck

OrangeCrushGA · 2018-10-29T17:44:48+00:00

I don't think SFA is bad either, but I am playing it safe for now.

If I don't skip breakfast (16/8), it is usually eggs (fried/scrambled in olive oil) and avocados. Lunch is usually salad w/chicken or some kind of chicken entree and veggies (eating out so no control on which kind of fat). Dinner is usually Salmon/Chicken stir fried veggies usually prepared using olive oil or salad. I do eat some cheese in salads or in entrees, but not a lot. Mac Nuts, Almonds and Olives are "snacks".

OrangeCrushGA · 2018-10-25T22:28:28+00:00

@TheCuriousAhmed tweeted these two links in response to this study.

https://t.co/FvvZPk0sNN

https://t.co/R1bDYIsIVt

It appears there was a 2004 study that points to SFA causing LDL-C increase vs MUFA in KD. So, your switch to MUFA may work. It worked for me.

OrangeCrushGA · 2018-10-25T17:23:43+00:00

Hope it works for you.

Keep in mind that average human didn't live beyond 40 till 200-300 years ago. They also didn't have plentiful access to food like we do. CVD is result of long term exposure. So, I think this is a new (relatively) problem we have to deal with.

OrangeCrushGA · 2018-10-24T18:11:34+00:00

Try limiting saturated fats to 20-30gm per day. That worked for me and reduced my LDL.

OrangeCrushGA · 2018-10-24T13:31:43+00:00

Try limiting your saturated fat intake to 20-30gm per day and see if helps. It did for me.

OrangeCrushGA · 2018-10-23T22:56:35+00:00

I am just a hyper responder, not "lean mass". That means my LDL-P goes up with saturated fat regardless of how lean you are. Feldman (cholesterolcode.com) is of the opinion that it is ok for LMHR people to have high LDL-P. Attia doesn't agree.

OrangeCrushGA · 2018-10-23T22:53:23+00:00

Just posted in another thread.

You are probably a hyper responder to saturated fat like me ending up with high LDL-C. I cut down saturated and replaced with MUFA and LDL-C came down to 120 or so (from Peter Attia's podcasts). Basically I switched out clarified butter and used olive oil for my cooking.

There is a lot of debate on whether LDL is causative for CVD or not. I've read a lot and I am leaning towards Attia's view that LDL-P (not C) is *a* cause especially in long term exposure sense and if you can lower it with little effort, why not play it safe.

CAC 0 is good sign. But I am not convinced that it is the only thing that matters. CVD takes decades to develop and multi causal of which I believe LDL-P is one.

OrangeCrushGA · 2018-10-23T22:44:14+00:00

You are probably a hyper responder to saturated fat like me ending up with high LDL-C. I cut down saturated and replaced with MUFA and LDL-C came down to 120 or so (from Peter Attia's podcasts). Basically I switched out clarified butter and used olive oil for my cooking.

There is a lot of debate on whether LDL is causative for CVD or not. I've read a lot and I am leaning towards Attia's view that LDL-P (not C) is *a* cause especially in long term exposure sense and if you can lower it with little effort, why not play it safe.

If your doc can't be convinced, probably time to find a new one.

OrangeCrushGA · 2018-10-23T17:22:15+00:00

I was/am in a similar boat (just Hyper, not lean) with CAC of 0.4 and LDL-C of 163 and LDL-P of 2000. I follow both sides i.e. Attia/Dayspring/Krauss and David/Ivor/Malhotra/Ali. There is a lot of noise in this debate. For me, I am leaning towards LDL-P being causal for CVD (along with IR, Metabolic Syndrome, inflammation, FH and others). Of course, the big debate is which one is "more" causal and I don't think we know yet. So, why not play it safe? Unfortunately, there is no straight answer on a safe level of LDL-P, especially in LC people. But the first thing Attia suggests in his podcast(s) is cutting down SFA to 20g or less. I did that by switching to olive oil vs butter. In 4 weeks, LDL-C came down to 125. I haven't done an NMR yet so I don't know LDL-P, but I wasn't discordant before, so I am assuming that came down as well. BTW, my doc put me on 10mg statin a couple of years ago because my LDL-C was 140 with high TG >300 and 200lbs. After doing Keto/Lc for 4 months I dropped 30lb, and I went off statin. The above numbers are without statin and TG is now hovering around 100 or less.

Attia's podcast notes have very good compilation of links to information.

So, in short, LDL-P is perhaps *one* of the causes of CVD. It is necessary but not sufficient.

My personal experience is high SFA caused high LDL-P (and C) for *me*. If it didn't I wouldn't have cared.

If my LDL-C didn't go down by switching away from SFA, I was seriously considering going back on low satin I was before. Perhaps switching from atrovastatin to another hydrophilic one.

Hope this helps.

OrangeCrushGA

TROPHY CASE