Yeah. Your numbers wouldn’t be concerning to me.
Run them in this risk calculator
https://cholesterolcode.com/report/

I think it will tell you you’re low or lowest risk.

No comment on your numbers, but here's a list of low-carb-friendly docs that might understand your situation a bit better than most:
https://www.lowcarbusa.org/low-carb-providers/lchf-doctors/

The first set of labs in 2015 after the first year on keto my cholesterol shot up some over 300. I have been low carb but not much keto for the past two years of working on improving my gut microbiome health.

My numbers have been dropping slowly for the past 5 years and the lab from last week showed a cholesterol of 247 and HDL of 56 giving me a ratio of 4.4 with 5 being middle of the road for a guy.

My calculated LDL was 175 which makes me pleased since I am over the age of 60 (being 69) as it seems to reduce my cancer risks and risks for death from all causes.

https://bmjopen.bmj.com/content/6/6/e010401

Is high LDL-C beneficial?
One hypothesis to address the inverse association between LDL-C and mortality is that low LDL-C increases susceptibility to fatal diseases. Support for this hypothesis is provided by animal and laboratory experiments from more than a dozen research groups which have shown that LDL binds to and inactivates a broad range of microorganisms and their toxic products.27 Diseases caused or aggravated by microorganisms may therefore occur more often in people with low cholesterol, as observed in many studies.28 In a meta-analysis of 19 cohort studies, for instance, performed by the National Heart, Lung and Blood Institute and including 68 406 deaths, TC was inversely associated with mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin.29 It is unlikely that these diseases caused the low TC, because the associations remained after the exclusion of deaths occurring during the first 5 years. In a study by Iribarren et al, more than 100 000 healthy individuals were followed for 15 years. At follow-up, those whose initial cholesterol level was lowest at the start had been hospitalised significantly more often because of an infectious disease that occurred later during the 15-year follow-up period.30 This study provides strong evidence that low cholesterol, recorded at a time when these people were healthy, could not have been caused by a disease they had not yet encountered.

Another explanation for an inverse association between LDL-C and mortality is that high cholesterol, and therefore high LDL-C, may protect against cancer. The reason may be that many cancer types are caused by viruses.31 Nine cohort studies including more than 140 000 individuals followed for 10–30 years have found an inverse association between cancer and TC measured at the start of the study, even after excluding deaths that occurred during the first 4 years.32 Furthermore, cholesterol-lowering experiments on rodents have resulted in cancer,33 and in several case–control studies of patients with cancer and controls matched for age and sex, significantly more patients with cancer have been on cholesterol-lowering treatment.32 In agreement with these findings, cancer mortality is significantly lower in individuals with familial hypercholesterolaemia.34

That high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction. This has been documented repeatedly without a reasonable explanation.35–37 In one of the studies,37 the authors concluded that LDL-C evidently should be lowered even more, but at a follow-up 3 years later mortality was twice as high among those whose LDL-C had been lowered the most compared with those whose cholesterol was unchanged or lowered only a little. If high LDL-C were the cause, the effect should have been the opposite.

Conclusions
Our review provides the first comprehensive analysis of the literature about the association between LDL-C and mortality in the elderly. Since the main goal of prevention of disease is prolongation of life, all-cause mortality is the most important outcome, and is also the most easily defined outcome and least subject to bias. The cholesterol hypothesis predicts that LDL-C will be associated with increased all-cause and CV mortality. Our review has shown either a lack of an association or an inverse association between LDL-C and both all-cause and CV mortality. The cholesterol hypothesis seems to be in conflict with most of Bradford Hill’s criteria for causation, because of its lack of consistency, biological gradient and coherence. Our review provides the basis for more research about the cause of atherosclerosis and CVD and also for a re-evaluation of the guidelines for cardiovascular prevention, in particular because the benefits from statin treatment have been exaggerated.38–40