After implementing certain health management practices, risk values can indeed change. By inputting new lifestyle data into the calculation module established by Phalanx, updated information can be obtained. However, since this function requires significant manpower and resources for development and maintenance, it is not currently available. Phalanx is working with strategic partners and hopes to provide this service in the future.

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Due to the research in this field, most group data accumulates over the past decade or so. With a responsible approach, we assert that predictions for the next ten years provide the most empirical evidence.

At the end of each report, the relevant genes used and their corresponding references are listed, allowing you to clearly check the scientific basis for the selected loci.

PMID and PMCID are reference numbers used by the PubMed and PubMed Central search engines, respectively. If you want to learn more about specific SNP disease risk research, you can visit the PubMed (http://www.ncbi.nlm.nih.gov/pubmed) or PubMed Central (www.ncbi.nlm.nih.gov/pmc/) websites. Enter the PMID or PMCID number in the search bar to read the abstract of the research article.

The report presents cancer risk as a concept of "relative risk." Your risk for Hodgkin's lymphoma is high, which means that your genetic predisposition and current exposure to environmental factors place you in a higher risk category relative to the population. However, since the overall incidence of Hodgkin's lymphoma is very low in the population, even if your risk is high, the actual incidence rate remains low. This situation is akin to being ranked last in an exam (high risk), but still achieving a high score of 90 (low incidence).

This situation indicates that you are exposed to multiple and significantly high-risk factors for esophageal cancer, such as alcohol metabolism gene ALDH2 SNP variations, smoking, alcohol consumption, and betel nut chewing. Studies have shown that when these high-risk factors are present simultaneously, there is an additive effect on the risk of esophageal cancer. Therefore, if your risk for esophageal cancer is significantly higher than for other cancers, it is advisable to avoid exposure to high-risk environmental factors (including smoking, alcohol consumption, betel nut chewing, and obesity).

Recent epidemiological studies have found that long-term smokers have a lower risk of developing Parkinson's disease compared to non-smokers. Some researchers hypothesize that certain chemicals in cigarettes, such as nicotine, may help protect the substantia nigra cells and prevent neurodegeneration. However, more clinical research is needed to confirm these findings. While smoking may reduce the risk of Parkinson's disease, it simultaneously increases the risk of many cancers and chronic diseases, so smoking is not recommended as a preventive measure for Parkinson's disease.

In many epidemiological studies abroad, smoking has indeed shown a tendency to reduce the risk of endometrial cancer, which is contrary to most other cancers. Since endometrial cancer is related to high levels of circulating estrogen in women and late menopause, some researchers speculate that the anti-estrogenic effects induced by smoking and early menopause may reduce the risk of endometrial cancer. However, the negative health impacts of smoking far outweigh its potential benefits, and smoking is not recommended as a preventive measure for endometrial cancer.

Many lung cancer patients have a smoking habit, which often leads to weight loss. Therefore, epidemiological studies have found that obese individuals, compared to those with a lower body weight, may actually have a relatively lower risk of developing lung cancer.

The SNP-based disease risk gene tests from different companies may use different SNP combinations and calculation methods, so their results may not be directly comparable.

Understanding disease risk is aimed at assessing the relative risk among populations and predicting the actual probability of occurrence to develop health management strategies. For the same SNPs, theoretically, one test is sufficient. However, the test provided by our company also includes a comprehensive evaluation of environmental risks. In the future, we plan to establish a feature that allows the input of new questionnaire data for re-calculating and re-evaluating the results. Additionally, based on the assessment results, routine medical check-ups can be conducted and adjusted in frequency as one of the management methods for monitoring specific high-risk diseases and their abnormalities.

In our computation model, it is indeed possible to estimate values for various age brackets based on current data. However, we primarily present data for the most recent ten-year range for two reasons: 1. The correlation between environmental risk factors and the current and next ten-year age brackets is strongest and thus more predictive. 2. Disease databases are typically categorized into ten-year intervals to reduce bias, and as time progresses, the incidence rates in these databases may change. Therefore, predicting for the closest ten-year interval is most effective.

1. The results of genetic factor testing will not change, but the values related to environmental risks may differ after interventions with preventive measures and health management methods.
2. The genetic factors theoretically do not need to be retested, but environmental factors can be reassessed by filling out a new questionnaire. This feature is currently under development.

The types and number of loci used by each company, as well as the evaluation logic they establish, can vary significantly, resulting in different levels of resolution. Additionally, the reference data included in each test may have slight variations in the criteria for defining disease scope, which could lead to differences in the results. To objectively evaluate, it is important to carefully compare the loci and logic used by each company.